Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Toxicology > Plants > Flashcards

Plants Flashcards

1
Q

Name and main system affected

A

Oleander (Nerium) Heart

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

Name and main system affected

A

Foxglove (Digitalis) Heart

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

Name and main system affected

A

Milkweed (Asclepias) Heart

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

Name and main system affected

A

Rhododendron, azalea, laurel (Rhododendron, Kalmia, Pieris) Heart

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

Name and main system affected

A

Yew (Taxus) Heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Name and main system affected

A

Death Camas (Zigadenus) Heart

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

Name and main system affected

A

Western False Hellebore (Veratrum) Heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Name and main system affected

A

Avocado (Persea) Heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Name and main system affected

A

Kalanchoe (Kalanchoe) Heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Name and main system affected

A

St. Johnswort, Klamath weed, goat weed (Hypericum) Skin - Primary photosensitizer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Name and main system affected

A

Allium spp - onions, garlic, chives, shallots Hemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Name and main system affected

A

Maple (Acer) Hemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Name and main system affected

A

Mustards (Cruciferae) Hemolysis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Name and main system affected

A

Sweet Clover (Melilotus) Hemostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Name and main system affected

A

Bracken Fern (Pteridium) Hemostasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Name and main system affected

A

Pine (pinus), Juniper (Juniperus), (Abies), (Pseudotsuga), (Picea), (Cupressus) Reproductive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Name and main system affected

A

Clover (Trifolium), Alfalfa (Medicago) Reproductive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Name and main system affected

A

Halogen (halogen), shamrock (oxalis) Kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Name and main system affected

A

Oak (Quercus) Kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Name and main system affected

A

Pigweed (Amaranthus) Kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Name and main system affected

A

Some lilies (lilium, hemerocallus) Kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Name and main system affected

A

Bleeding heart, Dutchman’s breeches (Dicentra) Nervous system stimulant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Name and main system affected

A

Water hemlock (Cicuta) Nervous system stimulant

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

Name and main system affected

A

Yellow star thistle (centauria), Russian knapweed (Acroptilion) Nervous system - mixed effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Name and main system affected

A

Locoweed (Astragalus) Nervous system - mixed effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Name and main system affected

A

Morning Glory (Ipomea) Nervous system - mixed effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Name and main system affected

A

Marijuana (Cannabis) Nervous System depressant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Name and main system affected

A

Jimson weed (Datura) Autonomic Nervous System

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Name and main system affected

A

Lupine (Lupinus) Autonomic Nervous System

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Name and main system affected

A

Poison Hemlock (Conium) Autonomic Nervous System

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Name and main system affected

A

Larkspur (Delphinium) Paralytic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Name and main system affected

A

Horsetail (Equisetum) Thiaminase containing plant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Name and main system affected

A

Cocklebur (Xanthium) Liver (2o photosensitizer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Name and main system affected

A

Tansy ragwort, groundsel (Senecio), Fiddleneck (Amsinckia), Houndstongue (Cynoglossum) Liver (2o photosensitizer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Name and main system affected

A

Alsike and red clover (Trillium) Liver (2o photosensitizer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Name and main system affected

A

Sago palm and cycad (cycas) Liver (2o photosensitizer)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Name and main system affected

A

Buttercup (ranunculus) GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Name and main system affected

A

English Ivy (Hedera) GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Name and main system affected

A

Bulbs (Narcissus, Iris, Hyacinthus, Amaryllis) GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Name and main system affected

A

Nightshade, Potato, Tomatoes (Solanum) GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Name and main system affected

A

Oxalate containing plants (dieffenbachia, philodendron, colocasia, mostera) GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

Name and main system affected

A

Castor bean (Ricinus) Gi tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Name and main system affected

A

Hairy vetch (Vicia villosa) Skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Name and main system affected

A

Black walnut (Juglans), Hoary alyssum (Berteroa) Skin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

Name and main system affected

A

Cyanogenic Glycosides Hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Name and main system affected

A

Flatweed Musculoskeletal - Stringhalt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

Name and main system affected

A

Moldy Sweet Potato Resp - Fog fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Name and main system affected

A

Perilla mint and mustards Resp - Fog fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Name and main system affected

A

Lush young green grass Resp - Fog fever

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

Plant characteristics of sweet clover?

A

Adult is tall and fragrant (3-9 feet)

Leaves are trifoliate and alternate.

Flowers are small and are yellow or white.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Toxic principle of Sweet Clover?

A

Coumarin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

Mechanism of action of sweet clover?

A

If sweet clover is put up wet, mold (aspergillus and others) on the clover causes coumarin to become dimeried and oxidized to dicoumarol (only the moldy/dry product is toxic, not fresh plant)

Dicoumarol interferes with vitamin K epoxide reductase

Interferes with clotting factors 2, 7, 9, and 10 and causes bleeding disorders and hemorrhage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

Animals affected by sweet clover and lesions seen?

A

Livestock, esp cattle

Bleeding disorders, hemorrhage

Signs, clinpath depend on site of bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

Treatment for sweet clover toxicity?

A

Supportive (Vitamin K1, fluids, blood transfusions, etc)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

6 toxins, MOAs, and clinical signs of mustard (cruciferae) toxicosis?

A
  1. Goitrin/thiocyanate - interfere with thyroid hormone synthesis and iodine uptake - goiter and young born weak and may die.
  2. Thiaminase-like activity or high sulfur - polioencephalomalacia and secondary copper deficiencies - lethargy, incoordination, muscle tremors, blindness, recumbancy, convulsion, death.
  3. S-methyl cysteine sulfoxide converted to dimethyl disulfide - hemolysis and Heinz bodies - jaundice, hemoglobinuria, anoreixa, splenomegaly, hepatic and renal hemosiderosis and degeneration/necrosis
  4. Equine Dysmaturity Syndrome - prolonged gestation but foal still immature with incomplete ossification, tendon ruptures, prognathism, etc.
  5. Bloat and other GI issues
  6. APEE and nitrate accumulation - reproductive inefficiency and enterotoxemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

How much sweet clover does an animal need to eat to see toxicity?

A

A LOT

Generally a historical problem, not seen much currently

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

How much mustard plants does an animal have to eat to see toxicity

A

Lots!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Toxic principle in maple leaves?

A

Unknown, but whatever it is it is only in the dry not the fresh leaves.

Seems to be most common in Red Maples?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Mechanism of action of maple leaves

A

Acute hemolytic anemia, methemoglobin, Heinz body formation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Species affected by maple leaf toxicity and lesions in those animals?

A

Mostly equine and alpaca

Technically all species susceptible

Hemolysis - icterus, splenomegaly, hepatomegaly (centrilobular degeneration), hemiglobinuric nephrosis.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

How many dried maple leaves does an animal need to eat to become toxic?

A

Lots.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Toxic principle in allium spp and where is it concentrated in the plant?

A

Numerous disulfides

Oxidizing agents

Most concentrated in the bulb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Mechanism of action of allium spp?

A

Oxidant damage of the red blood cells leads to Heinz body hemolytic anemia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Clinical signs of allium spp toxicosis?

A

Hemolysis that begins after a few days and peak at 5 days

Icterus, lethargy, odor to tissues, hemoglobinuric (hypoxic) necrosis chronically, abortions in cattle due to hypoxia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Species most susceptible to allium spp?

A

Cats, Cattle

Technically all animals susceptible but wide variation in susceptibilities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

Species most resistant to allium spp?

A

Sheep and goats

Technically all species susceptible but onions can be fed as 100% of diet to some sheep.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

Prognosis for animals with allium toxicosis?

A

Good with supportive care if the animal is not moribund.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

Of the allium spp, what is the most potent form?

A

Dried garlic!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

How much allium spp does an animal have to eat for toxicity?

A

Depends on the animal

Cat = small amount

Sheep = enormous amount

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

What are the 5 clinical diseases of bracken fern, and what species do these diseases present?

A
  1. Equine - neurotoxicosis from Type I thiaminase - weight loss with good appetite, incoordination, bradycardia, tremors/convulsions, recumbency, death.
  2. Bovine - Bone marrow suppression - first of the platelets causing bleeding disorders, last of the red blood cells causing weakness.
  3. Bovine - Enzootic hematuria - cyclic inflammation, urinary bladder papillomas, other neoplasms.
  4. Sheep - Retinal degeneration - glassy eyed appearance and dilated pupils.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

What are the toxic principles in bracken fern and where are they located in the plant?

A

Most toxic principle in young plants (fronds and crizomes) and rhizomes (green or dry) but technically is in all parts of the plant.

Equine diseases: Type I thiaminase

Cattle: Ptaquiloside

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Treatment for bracken fern toxicosis?

A

Ruminants: Antibiotics and supportive care

Equine/monogastrics: Thiaminase HCl

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

How much bracken fern does an animal need to eat for a toxic dose?

A

A lot!

25% of diet composed of fern for 3 weeks or more.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

How is bracken fern eaten by humans?

A

Fiddleheads are eaten.

Must cook to get rid of carcinogenic properties.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

What are some characteristics of the St. Johnswort plant?

A

Erect perennial found in dry sandy soils.

Leaves have small translucent glands in them.

Leaves are opposite one another.

5-petaled bright yellow flowers with small black dots along flower margins.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

What is the toxic principle in St. Johnswort?

A

Hypericin - a primary photodynamic pigment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

Which animals are affected by St. Johnswort and how much plant material do the animals have eat?

A

Any grazing animal.

Have to eat LOTS.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

Lesions caused by St. Johnswort?

A

Inflammation of the white areas of the skin, cornea, and conjunctiva.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

Why do humans take St. Johnswort? What effects can St. Johnswort ingestion have on humans?

A

Taken as a mood stimulant

Hyperforin inhibits many neurotransmitters including GABA.

Can interfere with the metabolism or excretion of over 50 drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

Cardiotoxins also generally have profound effects on what other bodily system?

A

The GI tract.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

What are some characteristics of oleander plant?

A

Evergreen found mainly in the SW US.

Long, narrow spear like leave with central veins, and very leathery

Flowers are brightly colored (any color but often pink)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

Toxic principle in oleander?

A

Cardiac glycosides (specifically oleandrin)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

Mechanism of action for oleander?

A

Cardiac glycosides inhibit Na/K ATPase which affects electrolyte distribution and so affects myocardial contractility and conduction.

May also increase vagal tone leading to bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

How much oleander does an animal need to eat to see toxicity?

A

Small amount!

5-10 leaves can be lethal to an adult cow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

How do grazing animals get access to oleander?

A

Generally by feeding animals tree clippings, lawn mower clippings, or by material getting into silage or hay

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

Clinical signs of oleander toxicity

A

Less than 8 hours: salivation, lethargy, diarrhea

Progresses to arrythmias, weakness, hypotension, bradycardia, dyspnea, coma, death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

Lesions of oleander toxicity

A

Myocardial vacuolation, degeneration, and necrosis

Ischemic renal necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

Diagnosis of oleander toxicity

A

Oleandrin residue analysis of GI contents and serum

ELISA test for digoxin may cross react with this test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

Treatment of oleander toxicosis

A

Toxins excreted slowly, so prolonged treatment (2-3 wks)

Multiple AC doses

Symptomatic care

Digibind: Digoxin specific Fab antibody fragments to bind toxin.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

How are humans commonly exposed to oleander?

A

Roasting food on oleander sticks while camping

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

What is more dangerous to dogs: dried oleander or fresh oleander?

A

Dry

Both have the same toxicity but dry is more palatable (bitter when fresh)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

Describe foxglove flowers

A

Bell shaped with dark spots on the inside.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

Toxic principle of foxglove and where it is found in the plant

A

Cardiac glycosides (specifically digoxin and digitoxin)

Found in entirety of plant

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

What animals are susceptible to foxglove toxicity?

A

All species

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

Mechanism of action for foxglove

A

Cardiac glycosides inhibit Na/K ATPase which affects electrolyte distribution and so affects myocardial contractility and conduction.

May also increase vagal tone causing bradycardia.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

Diagnosis of Foxglove toxicosis

A

Can use ELISA test for digoin on serum, blood, GI contents

Histological lesions on the myocardium (vacuolation, degeneration, and necrosis)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

Treatment of foxglove

A

Treat for 2-3 wks (toxin excreted slowly)

Multiple activated charcoal doses

Digibind: Digoxin-specific Fab antibody fragments to bind toxin

Symptomatic treatment.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

Where is foxglove native to?

A

Western Washington

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q

How much foxglove needs to be ingested for toxicosis?

A

Small amount

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

What is the toxic principle in Rhododendron, azaleas, laurels, and Japanese pieris?

A

Grayanotoxics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

Where in rhododendrons is toxin located?

A

Grayanotoxins in the entire plant but especially the leaves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
102
Q

Rhododendrons are toxic to all species, but in what species is toxicity most commonly seen?

A

Goats - clearing an area they mow down a lot of rhodies.

Toxicities also common if clippings given to other grazing animals.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
103
Q

What are the clinical signs of rhododendron toxicity?

A

PROMINENT GI SIGNS: Vomiting, anorexia, lethargy in 6 hours

24 hours: bradycardia, hypotension, dyspnea, recumbency, convulsions, death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
104
Q

How much rhododendron does an animal have to eat to see toxicosis?

A

Small amount

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
105
Q

Lesions for rhododendron toxicity

A

Gastroenteritis

Renal cortical and tubular necrosis from hypoxia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
106
Q

Diagnosis of rhododendron toxicity

A

History - or leaves easy to see in GI contents

Can test for grayanotoxins in GI contents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
107
Q

Treatment for rhododendron toxicosis?

A

IV lipid therapy

Decontaminate if possible

Supportive care for GI and heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
108
Q

What are the toxic principles in yew?

A

Taxines (one of ten types of alkaloids in yew)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
109
Q

What is the mechanism of action of yew?

A

Taxines interfere with myocardial conduction by affecting Ca and Na channels and altering intracellular K.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
110
Q

How much yew is toxic to an animal?

A

Small amount

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
111
Q

Clinical signs and when signs begin to occur?

A

Monogastrics: 15 minutes - 4 hours

Ruminants: Can be delayed, up to 38 hours

ACUTE CARDIAC FAILURE: trembling, dyspnea, ataxia, collapse, death.

May see some GI issues as well.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
112
Q

Lesions for yew toxicity?

A

None

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
113
Q

Diagnosis of yew toxicity

A

GI contents

Test contents for taxine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
114
Q

Treatment of yew toxicosis

A

Activated charcoal and cathartic

Supportive care for GI and heart

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
115
Q

Which part of the yew plant is toxic?

A

All except for the fruit of the berry (pink and fleshy, seed is toxic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
116
Q

Describe yew needles

A

Approximately 1 inch long

Dark on top, light on the bottom

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
117
Q

Why do people harvest yew bark?

A

Harvest taxol - has been used therapeutically as a breast cancer treatment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
118
Q

Describe death camas

A

Bulb looks like a wild onion but smells wrong and has a black covering.

Top part of the plant just looks like grass with thick blades and a strong V shape.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
119
Q

Toxic principle in death camas?

A

Steriod alkaloids (zygacine and others)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
120
Q

Where in death camas are toxins found?

A

Steriod alkaloids in all parts of the plant (esp problematic because top part can be grazed or harvested into hay)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
121
Q

Mechanism of action of death camas?

A

Peripheral vasodialtion and vagal stimulation leads to hypotension and bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
122
Q

Clinical signs of death camas

A

Within 6 hours, vomiting, salivation, muscle tremors, dyspnea, ataxia, weakness, convulsions, and death.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
123
Q

Diagnosis of death camas

A

Test for zygacine in GI contents

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
124
Q

Treatment of death camas

A

Supportive care for GI and heart

Activated charcoal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
125
Q

Where is death camas commonly found?

A

Montana and Idaho

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
126
Q

Why is milkweed called milkweed?

A

Generally has a milky sap in the stems and leaves that attracts butterflies.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
127
Q

What is the toxic principle in milkweed?

A

Cardiac glycosides and cardenolides.

Two species also have neurotoxins.

128
Q

What is the (main) mechanism of action of milkweed?

A

Cardiac glycosides inhibit Na/K ATPase which affects electrolyte distribution and so affects myocardial contractility and conduction.

129
Q

What are the clinical signs of milkweed toxicosis?

A

Heart signs: abrupt death, dyspnea, tachycardia, etc.

Other toxins in the plant may cause GIT, respiratory system, or nervous system signs.

Also causes skin irritation

130
Q

How much milkweed does it take to be toxic to an animal?

A

Depends on species sensitivity (all animals susceptible)

Moderate amount (about 1 kg) for a horse

Small amount for a sheep.

131
Q

Treatment for milkweed toxicosis

A

Sedatives, analgesics, other supportive care based on clinical signs.

Control is easy as milkweed tends to grow an obvious, solitary plant.

132
Q

Describe kalanchoe

A

Houseplant often seen in grocery stores

thick succulent leaves.

Flowers = clusters, bright, long lasting blooms, 4-petalled.

133
Q

Toxic principle in kalanchoe, and where is it found

A

Cardiac glycosides

Found in all parts of the plant but esp. the flowers

134
Q

How much kalanchoe is toxic to animals?

A

Pretty large amount

135
Q

Clinical signs of kalanchoe

A

GIT upset in a few hours

Arrythmias, tacycardia, dyspnea if dose is high enough, cardiac arrest at extreme end.

136
Q

What is the main lesion associated with kalanchoe?

A

Gastroenteritis

137
Q

Treatment for kalanchoe

A

Emesis, AC

Supportive care (fluids, antiarrythmic drugs, etc.)

138
Q

What species are susceptible to avocadoes?

A

BIRDS

All spp technically susceptible but birds are really the only species we see serious toxicosis in.

139
Q

What is the toxic principle of avocado and where in the plant is it found?

A

Persin

All parts of the plant

140
Q

Clinical signs of avocado toxicosis?

A

Avian: acute respiratory and cardiac distress

Lactating animals: Non-infectious mastitis and myocardial necrosis.

Horses: Edema of the head and neck which may cause ischemic myopathy / ischemic myelomalacia.

141
Q

Describe the characteristics of western false hellebore

A

Large alternating leaves with parallel veins

Produce flowers on a thick unbranched stem

Found in very moist areas.

Smells skunky to most people.

142
Q

What is the toxic principle of Western False Hellebore?

A

Glycoalkaloids and Ester alkaloids

143
Q

Where is toxic principle located in Western False Hellebore?

A

Concentrated in the young shoots and roots

Decreased concentration in mature leaves

144
Q

What is the mechanism of action of Western False Hellebore?

A

Heart: Bradycardia from increased vagal tone and Hypotension from peripheral vasodilation.

Teratogenic: 5 alkaloids

145
Q

How much Western False Hellebore does the animal eat to see toxicity?

A

Teratogenesis: Only a little

Lethality: A lot

146
Q

What are the effects of Western False Hellebore as a teratogen?

A

Depends on dose and the stage of gestation.

Early embryonic death/Abortions, Cyclopia, Cleft Palate, Arthrogryposis, Tracheal Stenosis, Vertebral column deformities (lordosis, kyphosis, scoliosis)

147
Q

What are the clinical signs of Western False Hellebore as a cardiotoxin?

A

GI: Salivation, Vomiting/Regurgitation

Cardio: Weakness, incoordintation, bradycardia, hypotension, convulsions, coma, death.

148
Q

Treatment for Western False Hellebore

A

None

In adult animals, if source is removed should be self-limiting in 3-4 hours.

Only treatment for pregnant animals = prevention

149
Q

What evergreen needle trees have the highest concentration of toxin and how do you recognize them?

A

Pondarosa pine: long needles in clusters of 3.

Lodgepole pine: long needles in pairs.

Over 25 spp. have toxin but in lower levels and generally unpalatable so not many toxicities seen.

150
Q

Toxic priniciple in pines? Where is it found?

A

Isocupressic Acid

In bark and needles.

151
Q

Mechanism of action of pines?

A

Isocupressic acid = TONE GENERATING COMPOUND

Causes uterine vasoconstriction (esp. of the uterine artery)

Fetus releases cortisol causing abortion/premature partruition

Often see retained placentas

152
Q

What stage of gestation are pine needles a biggest problem for?

A

Risk highest in the last trimester, but fetuses can also be affected in the first or second trimester.

153
Q

How much pine needs to be eaten to see toxicity in animals.

A

A large amount.

154
Q

What species are most susceptible to pine needle toxicity?

A

Cattle

155
Q

Lesions from pine needle toxicity?

A

Vasoconstricution of caruncles with necrosis and hemorrhage.

156
Q

Diagnosis of pine needle toxicity

A

Test fetal thoracic fluid and fetal GI contents for tetrahydroagathic acid (metabolite of isocupressive acid)

May also be able to test uterine artery

157
Q

Prevention of pine needle toxicity

A

Don’t graze cattle in pine forests

Provide low protein/high energy diet = experimentally produces avoidance

158
Q

For what species can alfalfa and red clover be toxic?

A

Most signs are mainly in ruminants

Slobbering disease in all species

159
Q

What the toxic principles/clinical syndromes seen with alfalfa/redclover toxicity?

A

Saponin / proteins can cause bloat

Estrogen / coumesterol can cause infertility or cystic ovaries

Unknown agent can cause photosensitivity

Slaframine can cause slobbering disease

160
Q

Describe halogeton

A

Reddish stem

Tubular sausage-like fleshy green gray leaves arranged in clumps

Gen in alkaline, dry soil

161
Q

What plant has the same toxic principles as halogeton?

A

Shamrock (Oxalis)

(4-leaved clover type plant often with a purplish center)

162
Q

Toxic principle of halogeton?

A

Soluble sodium and potassium oxalates

163
Q

How much halogeton does an animal need to ingest to see toxicity?

A

Moderate amount

164
Q

In what species is halogeton toxicity most commonly seen in and why?

A

Grazing animals (esp sheep and cattle) during the winter - dried plants stick up out of the snow and are palatable, and toxin concentrated in the dry plants.

165
Q

Mechanism of action of halogeton

A

Soluble oxalates are a metabolic poison - interfere with lactate and succinate dehydrogenase

Oxalates bind Ca2+ and so cause hypocalcemia

Formation of calcium oxalate crystals in the renal tubles cause renal necrosis

166
Q

Clinical signs of halogeton?

A

Generalized hypocalcemic signs early: salivation, lethargy, dyspnea, ataxia, muscle tremors, seizures

Renal signs later

167
Q

Clin Path and Lesions of halogeton

A

Clin Path: hypocalcemia and azotemia

Renal tubular necrosis due to calcium oxalate crystals

168
Q

Treatment of halogeton?

A

Give dicalcium phosphate orally so that oxalates will be bound in the gut and not get absorbed as much.

169
Q

Toxic principle of oak and where is it found?

A

Gallotannins (gallic acid, tannic acid, pyrogallol)

Found in acorns and budding/immature leaves

170
Q

How much oak does an animal need to eat to see toxicity?

A

Lots and lots

171
Q

Clinical signs of oak toxicity?

A

GI: bloody, mucoid diarrhea

Renal: weakness, weight loss, lethargy, eventual death.

172
Q

Clinical Pathology of Oak toxicosis

A

Isosthenuria, proteinuria, azotemia, hyperkalemia, hypoproteinemia, hypocalcemia.

173
Q

Lesions of oak toxicity

A

Gastroenteritis

Nephritis - multifocal necrosis of proximal renal tubules

+/ edema, ascites, etc.

174
Q

Prognois for oak toxicity?

A

Generally poor - renal damage irreversible

175
Q

Toxic principle of pigweed

A

Nitrate accumulator

Also contains soluble oxalates

176
Q

Treatment for pigweed

A

Renal = supportive

Nitrates = methylene blue

177
Q

What are the two types of lillies that are nephrotoxic?

A

Lillium and Hemerocallus

(Tiger lily, Easter lily, Day lily, Asiatic hybrid lily, Stargazer lily)

178
Q

What is the toxic principle in nephrotoxic lilies and where is it located?

A

Unknown but definitely water soluble

All parts of lily

179
Q

How much lily does an animal need to eat to see toxicity

A

Tiny amount (a bite)

180
Q

In what animals are lilies toxic?

A

CATS only

(Dogs can have some GI upset from the bulb)

181
Q

Clinical signs of lily toxicity

A

GI upset

Renal signs in 48-96 hours!

May see facial and paw edema

182
Q

Lesions of lily toxicity

A

Severe acute renal tubular necrosis

NO oxalate crystals

183
Q

Treatment of lily toxicosis

A

Decontaminate! Emesis, AC, cathartic, etc.

IV fluid diuresis for 48-72 hours

Monitor renal values

184
Q

What is the toxic principle of bleeding heart and where is it found?

A

Isoquinoline-like alkaloids

In all parts of the plant

185
Q

Clinical signs of bleeding heart toxicity?

A

Gastrointestinal signs first

Muscle tremors, prostration, convulsions.

186
Q

Prognosis for bleeding heart toxicity?

A

Usually good - death is very rare and recovery is rapid.

187
Q

Treatment for bleeding heart toxicosis?

A

Generally none - animals recover in less than 2 hours in most cases.

188
Q

Describe some characteristics of water hemlock

A

Bulbous root with yellow resin in very moist areas or in water.

Adult plant can be 3-10 feet tall with a hollow stem.

Umbrella like clusters of white flowers

189
Q

Toxic principle in water hemlock and where it is found

A

Cicutoxin

Mostly in roots and young shoots

190
Q

How much water hemlock does an animal need to eat to see toxicosis?

A

Small amt (one root can kill pretty much any animal)

191
Q

Clinical signs of water hemlock toxicosis

A

Rapid onset in 15-45 minutes: first pre-ictal uneasiness then violent convulsions and death.

192
Q

Diagnosis of water hemlock toxicity?

A

Generally still see the plants in the GI contents because death is so rapid.

Can also test for cicutoxin in GI contents.

193
Q

Prognosis for water hemlock toxicity?

A

Grave - fatality so fast.

194
Q

Describe some characteristics of yellow starthistle

A

1-3 feet tall

Thin, short, narrow leaves that almost look like needles

Stem and leaves covered with cottony hair

Oviod spiny flower base

195
Q

Toxic principle of yellow starthistle and where it is located

A

Pyrone (hypothesized)

Found only in aerial portions of the plant

196
Q

What species is yellow starthistle a problem?

A

Horses and other equids

197
Q

What lesion does Yellow Starthistle cause and what nerves does this lesion affect?

A

Nigropalladial encephalomalacia

Impairs CN: 5, 7, 9, 12. (Trigeminal, Facial, Glossopharyngeal, Hypoglossal)

198
Q

How much yellow starthistle does an animal have to see for toxicity?

A

A LOT.

199
Q

Mechanism of action of Yellow Starthistle

A

Binds to dopaminergic receptors and causes necrosis. (Hits same receptors as cocaine does, some young horses seem to be addicted to it)

Dopaminergic areas: Anterior globus palladius, substantia nigra.

200
Q

Clinical signs of yellow starthistle toxicity

A

Acute presentation of a chronic problem

Lip twitching, involuntary chewing movements.

Trouble eating and drinking = starvation (wasting, death)

201
Q

Prognosis for yellow starthistle toxicity?

A

Grave. Not reversible.

202
Q

Toxic principles in Locoweed (3)

A
  1. Miserotoxin - in all parts of the plant only when FRESH.
  2. Swainsonine/Swainsonine-N-oxide - mainly in the seeds, thought to be a mycotoxin.
  3. Selenium accumulator
203
Q

Mechanism of action of locoweed

A

Miserotoxin: Both neuro and respiratory effects

Swainsonine (and S-N-Oxide) inhibit Golgi mannosidases which leads to the accumulation of mannose in cytoplasma and vacuoles/lysosomes of neurons, hepatocytes, renal tubules, and other tissues.

Selenium: causes skin and abortions.

204
Q

Clinical signs of locoweed

A

Miserotoxin: ataxia (Wallerian degeneration of peripheral nerves and posterior spinal cord), pulmonary edema and emphysema, death.

Swainsonine: Locoism - ataxia, visual impairment, hyperexcitability or lethargy, emaciation.

Selenium: Hoof and hair problems, abortions, unthriftiness.

205
Q

Diagnosis of locoweed

A

Can test for swainsonine

Can also evaluate mannoidase activity (for decrease)

206
Q

Histological lesions of locoweed

A

Vacuolization of many cell types including neurons, renal epithelial cells, hepatocytes

207
Q

Toxic principle in morning glory and where it is located

A

Lysergic acid derivatives

Only in the seeds

208
Q

How many morning glory seeds does an animal have to eat to see toxicosis?

A

A LOT.

209
Q

Clinical signs of morning glory toxicosis?

A

Vomiting, diarrhea, dilated pupils, hallucinations, disorientation, other bizzare behavior

210
Q

Treatment of morning glory toxicosis?

A

Supportive care +/- sedation.

211
Q

What do you always have to worry about with a pet that came in for eating marijuana?

A

Dual exposures!! (xylitol, raisins, chocolate, macademia nuts).

212
Q

Toxic principle of marijuana?

A

THC - tetrahydrocannabinols

213
Q

Mechanism of action of marijuana

A

CNS depression and derangement

214
Q

Clinical signs of marijuana toxicosis

A

Ataxia, lethargy, dilated pupils, easily aroused, inappropriate urination, changes in heart rate, hyperexcitability, inappropriate urination.

215
Q

Prognosis for marijuana toxicity

A

Good - fatalities very rare and so far only seen with dual toxicities

216
Q

Treatment for marijuana toxicity

A

IV lipid therapy for very high exposures

Decontamination

Supportive care

217
Q

What does the fruit and leaves of a trumpet vine look like?

A

Fruit = round, spiny

Leaves = simple, alternating, strong odor.

218
Q

What are the toxic principles in trumpet vine?(3) Where are they?

A
  1. Atropine
  2. Hyoscyamine
  3. Scopolamine

All parts of the plants toxic but especially the seeds.

219
Q

Clinical signs of trumpet vine toxicity?

A

Trembling, excitation, colic, dilated pupils, tacky mucous membranes, tachycardia, blurred vision, decreased intestinal motility

220
Q

Treatment for trumpet vine toxicity

A

Decontamination

Physostigmine should theoretically work but not much clinical success

221
Q

Toxic principles of lupine and which type of plant has most?

A

Guinolizidine alkaloids

“Bitter” lupines have more alkaloids than “sweet” lupines

222
Q

Lupine mechanism of action

A

A nicotinic effect - mimicing acetylcholine at both sympathetic and parasympathetic ganglia, NMJs, and CNS.

This acts as an anesthetic for the growing fetus

223
Q

What are the clinical signs of lupine in fetal cattle?

A

Crooked Calf disease: Arthrogryposis, Vertebral column abnormalities (kypohosis, lordosis, scoliosis), Cleft Palate.

Rarely may kill the calf and cause abortions

224
Q

What is the critical time period for malformations in a cow eating lupine?

A

Day 40-110 of gestation

225
Q

How much lupine does an animal need to eat for toxicity?

A

Generally occurs in animals that eat a LOT but in only a short period of time

226
Q

What is the essential characteristics of poison hemlock?

A

Purple spots! (on the stem)

Otherwise looks very similar to water hemlock except in dry land instead of water.

227
Q

Toxic principle in poison hemlock and where it is located

A

Piperidine alkaloids

In the whole plant, increasing in concentration as the plant matures.

228
Q

How much poison hemlock does an animal need to eat to see toxicity?

A

Small amount

229
Q

Mechanism of action of poison hemlock

A

Nicotinic effects (like lupine) can theoretically cause anesthetic effects and fetal malformations.

230
Q

What animal is most commonly poisoned by poison hemlock?

A

Humans! Root looks like a carrot.

Then cattle.

231
Q

Clinical signs of poison hemlock?

A

Muscle tremors, weakness, ataxia and DUMBSLED signs (salivation, lacrimatin, defecation)

Respiratory arrest

Rare: can see arthrogryposis, cleft palate, and vertebral column abnormalities.

232
Q

Toxic principle of larkspur?

A

Polycyclic diterpene alkaloids

233
Q

When is larkspur most dangerous?

A

When the plant is the most palatable - from the pre-blooming to the pod-forming stage

234
Q

Mechanism of action of larkspur

A

Paralysis: Inhibition of the post-synaptic neuromuscular junction by acting as a competative inhibitor of Acetylcholine. Bind more tightly to nicotinic acetylcholine receptors than others.

235
Q

Clinical signs of larkspur

A

Most commonly, cattle just found dead on pasture (acute death)

May see uneasiness, ataxia, muscle stiffness, muscle twitching, and abdominal pain.

236
Q

Treatment of larkspur

A

May be able to treat with physostigmine to increase the Ach in the NMJ

Can also use neostigmine for the same reason

237
Q

Prevention of larkspur toxicity?

A

Graze only when the plant is not palatable (later in the season after pods formed)

Lithim supplements may induce larkspur refusal?

238
Q

Toxic principle in horsetail and where in the plant?

A

Thiaminase-like compounds (breaks down Vit B1)

All parts of the plant

239
Q

How much horsetail does an animal have to eat to see toxicosis?

A

Lots!

240
Q

What species are primarily affected by horsetail?

A

Horses!

241
Q

Clinical signs of horsetail toxicosis?

A

Like polioencephalomalacia (but no gross lesions!)

Weakness, weight loss despite good appetite, hind limb ataxia or paralysis, convulsions, possibly death.

242
Q

Prognosis for horsetail toxicosis?

A

Good if animal is not yet recumbant.

243
Q

Treatment for horsetail toxicosis?

A

Thiamine HCl (aka, Vitamin B1)

244
Q

What do the spines on a cockleburr look like?

A

Curved and hooked!

245
Q

Toxic principle in cockleburr and where is it found?

A

Carboxyatractyloside

Found in the seeds within the burr and the dicotyledons (babies) as they grow.

246
Q

How much cockleburr does it take for toxicity?

A

Moderate amount

247
Q

Clinical signs of cockleburr toxicosis?

A

12 hours to 2 days: Anorexia, weakness, lethargy, nausea, vomiting, dyspnea, muscle contractions, convulsions, death

Ascites

248
Q

Pathological lesions of cockleburr toxicity?

A

Mottling of the liver and kidney (due to degeneration/necrosis)

GIT inflammation

IN SWINE ONLY: neuronal degeneration and necrosis

249
Q

Why is cockleburr an uncommon toxicity?

A

The burrs are so hard that it is often hard for the animals to get to the seeds. Most commonly a problem when the burrs are cut up and then incorporated into silages and hays.

250
Q

Name some of the pyrrolizidine alkaloid containing plants (common names)

A

Tansy Ragwort

Groundsel

Hound’s Tongue

Tarweed

Fiddleneck

251
Q

How much of a plant containing pyrrolizidine alkaloids would an animal have to eat to see a toxicity?

A

Lots!

TOXICITY IS CUMULATIVE

252
Q

Animals susceptible to pyrrolizidine toxicities

A

Cattle, horses, pigs, poultry

253
Q

Animals resistant to pyrrolizidine alkaloid toxicities

A

Sheep and goats (and likely camelids)

254
Q

Mechanism of action of pyrrolizidine alkaloids

A

Metabolized to highly active pyrroles

Pyrroles alkalate DNA and impairs cell division

Cell continues to grow until critical mass is reached and then necrosis of the cell occurs

255
Q

Lesions of pyrrolizidine alkaloid toxicosis

A

Grossly liver can be large or small.

Histo: hepatic megalocytosis, centrilobular necrosis, bile duct proliferation, and portal fibrosis

256
Q

Clinical signs of pyrrolizidine alkaloid toxicity

A

Classic hepatic failure signs + secondary photosensitization and hepatic encephalopathy

257
Q

Diagnosis of pyrrolizidine alkaloid toxicity

A

This is the primary cause of megalocytosis (though not pathognomonic)

Can test liver and blood in early stages but this is unreliable.

258
Q

What is the toxic principle in alsike/red clover?

A

Unknown principle can cause liver damage.
Slaframine = slobbering disease

259
Q

Clinical signs of red/alsike clover toxicity

A

Depending on dose may see secondary photosensitization or hepatic encephalopathy and other liver signs.

Slobbering disease in any animal.

260
Q

Lesions of red/alsike clover toxicity

A

Hepatomegaly, perilobular fibrosis and bile duct proliferation.

261
Q

Prognosis of red/alsike clover toxicity?

A

Depends on the amount of liver damage it has caused.

262
Q

In what species is liver damage seen with red/alsike clovers?

A

Liver damage ONLY in horses

(slobbering disease in all animals)

263
Q

What are the toxic principles in sago palm? (3) And where are they in the plant?

A
  1. Cycasin (and metabolite methylazoxymethanol) - liver
  2. Beta-methylamino-L-alanine - nervous system
  3. Unknown

All parts toxic, female parts more so, seeds and nuts are most toxic.

264
Q

Clinical signs of sago palm toxicity and when they occur

A

15 min: Intense GI signs

2-3 days: hepatic and nervous signs.

265
Q

In what species are sago palm toxicities most commonly seen?

A

Theoretically can affect all species but 90% of toxicities in dogs.

266
Q

Lesions of sago palm toxicosis?

A

Focal centrilobular and midzonal necrosis

267
Q

Treatment of sago palm toxicosis

A

Decontaminate + multiple AC doses

GI and liver protectants

Monitor chemistry panels

Supportive care

268
Q

Toxic principle in buttercup and where is it?

A

Ranunculin converted to GI irritant, protoanemonin.

In entire plant but only when fresh.

269
Q

How much buttercup does an animal need to ingest to see toxicosis?

A

A lot

270
Q

Clinical signs of buttercup toxicosis?

A

Often see dermatitis (esp in humans)

GI issues mainly

In some spp: muscle weakness, difficulty breathing (esp sheep)

271
Q

Toxic principles in English Ivy (3) and where they are?

A

All parts of the plant, esp the berries

  1. Triterpenoid
  2. Saponin
  3. Hederagenin
272
Q

Clinical signs for English Ivy Toxicity

A

Severe GI signs: salivation, vomiting, diarrhea.

273
Q

Prognosis for English Ivy toxicosis

A

Good - fatalities are rare.

274
Q

Which bulbs cause GI symptoms?

A

Lots - tulips, iris, amaryllis, hyacinth!

275
Q

Toxic principle in tulip bulbs

A

Alkaloids

276
Q

Clinical signs of tulip bulb toxicity

A

Oral irritation and mild or severe gastroenteritis

Rarely serious

277
Q

What domestic plants are related to nightshade?

A

Tomato and potato

278
Q

Toxic principle and mechanism of action in nightshade?

A

Solanine

This is converted to a sugar or solanidine which affects the purkinje cells of the cerebellum

Some plants contain atropine

279
Q

Clinical signs of nightshade toxicity?

A

GI signs

Nervous signs: dyspnea, ataxia, paresis or paralysis

DUMBSLED signs if atropine containing plant

280
Q

How much nightshade does an animal have to eat for it to be toxic?

A

Lots

281
Q

What kind of plants are insoluble oxalate containing plants typically?

A

House plants

Generally dark green with large broad leaves.

282
Q

What are the toxic principles in insoluble oxalate plants?

A

Insoluble oxalates and proteolytic enzymes

283
Q

Mechanism of action of insoluble oxalate containing plants?

A

Oxalate crystals irritate the GI mucosa

Proteolytic enzymes trigger the release of kinins and histamines

284
Q

Clinical signs of insoluble oxalate containing plants?

A

Salivation, swelling of the oral mucosa

Vomiting and diarrhea

285
Q

Treatment for insoluble oxalate containing plants?

A

Supportive, esp. rinsing the mouth and giving fluids.

Often includes anti-histamines to quell release.

286
Q

Prognosis for insoluble oxalate plants?

A

Good

287
Q

If death does occur from insoluble oxalate containing plants, why does it occur?

A

Hypoxia from swelling of the airways

288
Q

How do pets get castor beans?

A

Either from gardens or a lot of times found in jewelry.

289
Q

Toxic principle in castor beans and where it is located?

A

Ricin (water soluble and rapidly absorbed)

In the seed inside of the outer shell

290
Q

How many castor beans are needed to cause toxicity?

A

Small amount! Just one for a dog.

291
Q

How can castor beans be used as a biological weapon?

A

If aerosolized and inhaled, ricin will cause pulmonary pathology

292
Q

Clinical signs of castor bean toxicity?

A

GI distress in 12-48 hours

If high enough does, multi-systemic problems: hypotension, muscle twitching, dyspnea, convulsions, coma, death.

293
Q

Lesions with castor bean toxicosis?

A

Gastroenteritis

Hepatic, renal, or myocardial necrosis

294
Q

Treatment for castor bean toxicosis?

A

Only supportive

295
Q

Characteristics of hairy vetch?

A

Terminal tendrils on the end of each vine

Pea-like flowers and seed pods

296
Q

Toxic principle of hairy vetch?

A

Unknown

297
Q

Species commonly affected by hairy vetch?

A

Cattle and horses

298
Q

Clinical disease from hairy vetch?

A

There are four but most commonly seen is systemic granulomatous disease.

299
Q

How much hairy vetch needed to see toxicity?

A

A lot!

300
Q

Pathologic lesions associated with hairy vetch

A

Multiple granulocytic lesions (eosinic, lymphocytic, or plasmacytic infiltrate with multinucleated giant cells)

Dermatitis and conjunctivitis

301
Q

Mechanism of action for hairy vetch?

A

Granulomas due to a Type IV hypersensitivity reaction.

302
Q

What is the toxic principle for hoary alyssum?

A

Unknown

303
Q

What plant has the same mechanism of action as hoary alyssum?

A

Black walnut

304
Q

What animals are affected by hoary alyssum/black walnut toxicity?

A

Equine

305
Q

Clinical signs of black walnut toxicity?

A

Limb edema, laminitis, and fever if INGESTED

306
Q

What happens when dogs ingest black walnut WOOD?

A

Can see neurologic or musculoskeletal signs - vomiting, lethargy, hind limb weakness, tremors, ataxia, disorientation, pain, seizures

307
Q

What are the clinical signs of dogs eating black walnuts themselves or the hulls of black walnuts?

A

GI signs - salivation, vomiting, anorexia, diarrhea.

308
Q

Should you use fat or water to clean off poison oak/poison ivy lesions?

A

Both! Toxin is lipid soluble but plant water soluble.

309
Q

What are some examples of cyanogenic glycoside containing plants?

A

Chokecherries, apple seeds, cherry pits, most other seed fruits.

310
Q

What is the mechanism of action of cyanogenic glycosides?

A

Cyanogenic glycosides broken down to sugar and aglycone (by beta-glycosidase)

Aglycone converted to hydrocyanic acid (by hydroxynitrile lyase)

Cyanide interacts with ferric iron of cytochrome oxidase, which inhibits electron transport and cellular respiraton.

Blood is fully oxygenated but cannot be utilized by the cells.

311
Q

Clinical signs of cyanogenic glycoside toxicity?

A

Salivation

Hyperpnea, Dyspnea - death from respiratory paralysis

Weakness and muscle fasciculations, convulsions

Blood may be bright cherry red but rarely observed clinically.

312
Q

Pathologic lesions of cyanogenic glycosides

A

Bright red mucous membranes

“Bitter almond” smell to GI contents

313
Q

Treatment of cyanogenic glycoside toxicity

A

Cyanokit - contains hydroxocobalamin (precursor to B12) to bind cyanide and have it be eliminated by the urine.

Other care = supportive

314
Q

What can flatweed cause?

A

Stringhalt

315
Q

Name four plants that can cause fog fever (pulmonary emphysema and edema), and how each can cause it.

A

Lush greens in early spring - contains high levels of tryptophan which is converted to 3-methyl indole in the rumen. 3-MI affects the lungs.

Moldy Sweet Potato - produces 4-ipomeanol, affects the lungs.

Perilla mint

Mustards

Toxicology (1 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions