Poisonous Plants - Exam 2 Part 2 Flashcards

1
Q

Nephrotoxins/oxalate poisoning MOA

A

oxalate precipitates calcium, inhibiting lactate & succinic dehydrogenase resulting in oxalate nephrosis

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2
Q

clinical signs of oxalate poisoning

A

kidney failure
tetany, muscle tremors, weakness, recumbency
blood tinged nasal discharge
coma & death (12 hours)

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3
Q

diagnostic signs of oxalate poisoning

A

hypocalcemia
renal tubular necrosis & oxalate crystals
hemorrhage/hyperemia
rumen wall hemorrhage/edema

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4
Q

treatment for oxalate poisoning

A

calcium borogluconate hydration

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5
Q

prevention for oxalate poisoning

A

Calcium Phosphate mineral supplement
water before moving into oxalate rangelands
gradual introduction to halogeton grazing

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6
Q

oxalate poisoning causing plants

A
  1. halogeton w/ greasewood
  2. oxalis spp. - shamrock, sorrel, soursob
  3. red-rooted pigweed
  4. Kochia weed
  5. curly leaved-dock
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7
Q

Oaks - Quercus spp.
toxin:
most susceptible spp
most resistant spp

A

toxin: Gallotannins (denature of cellular proteins (astringent))
cattle, sheep, horses, pigs
goats resistant due to tannin binding salivary proteins & tannase activity

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8
Q

oak toxicity diagnostic signs

A

elevated liver enzymes, BUN, creatinine, K+
pale swollen kidneys with tubular necrosis and hyaline casts
liver necrosis

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9
Q

oak toxicity clinical signs

A

icterus, azotemia, red-brown urine, tarry diarrhea, abdominal pain, hemorrhagic enteritis

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10
Q

Cockle bur toxicity
toxin
most toxic part of plant
MOA
clinical signs

A

toxin: carboxyactractyloside
seeds, 2-leafed cotyledons
inhibits oxidative phosphorylation
hypoglycemia, elevated liver enzymes, convulsions, hunched back, ataxia, recumbent

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11
Q

cockle bur most toxic part of the plant

A

seeds, 2-leafed cotyledons

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12
Q

What is the plant that induces calcinosis in North America?

A

day-blooming jasmine

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13
Q

What is the mechanism of action of plant induced calcinosis in North America?

A

analog of vitamin D → hypercalcemia → calcification of tendons, ligaments & arteries, stiffness/lameness, increased bone density

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14
Q

What are 2 major plants associated with tremetol induced myopathy/neurotoxicity?

A

White SnakeRoot & Rayless GoldenRod

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15
Q

what are the clinical signs associated with tremetol induced myopathy and neurotoxicity?

A

“milk sickness”, myoglobinuria, “choke”, cardiomyopathy, heartblock/death, elevated liver enzymes

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16
Q

what is the association with horses and black walnut shavings?

A

laminitis

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17
Q

Se toxicity MOA

A

Se replaces sulfur in proteins → inhibits function, depletes S-adenosylmethionine, GSH → oxidative stress

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18
Q

Se toxicity clinical signs

A

hair loss of tail, lameness, hoof lesions, depression, anemia, emaciation, diarrhea, reproductive abnormalities, death

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19
Q

Know toxic levels in blood, hoofs, liver for Se toxicity.

A

blood > 1 ppm
hoofs > 5 ppm
liver > 5 ppm

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20
Q

Why is whole blood better for diagnosis of Se toxicity? Could serum levels be normal in an animal with hoof and hair lesions?

A

Whole blood > serum as ⅔ of blood Se is in the RBC (metabolized by RBC first)

Yes serum levels could be normal?

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21
Q

6 common selenium accumulating plants

A

prince plume
woody aster
paint brush
2-grooved milkvetch
4-winged saltbush
gum weed

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22
Q

Identify 5 plants associated with intestinal obstruction.

A

Simon gets obstructed by sugar beats and beans in China
1. persimon fruits
2. sugar beat tops
3. mesquite beans/pods
4. mescalbean beans/pods
5. chinaberry

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23
Q

what are buttercups associated with?

A

protoanemonin toxicity

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24
Q

protoanemonin toxicity clinical signs

A

oral mucosa irritant, EXCESSIVE SALIVATION, gastroenteritis, colic, diarrhea, hemorrhagic diarrhea

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25
Q

Describe the components found in legumes (Yellow sweet closer & Alfalfa) that contribute to rumen bloat

A

high protein - foaming
saponins - stabilize foam
high Ca2+ - increase surface tension

increased by acidity

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26
Q

Identify plants, clinical signs associated with spewing sickness.

A

orange sneezeweed
bitterweeds
colorado rubberweed

27
Q

spewing sickness clinical signs

A

Digestive: vomiting, bloat, anorexia, abdominal pain
Liver: liver degeneration and elevated enzymes
aspiration pneumonia/coughing, DEATH FROM INHALED VOMIT

28
Q

what is colic associated with

A

GI irritants and alkaloids with Atropine-like action

29
Q

toxin of nightshade poisoning

A

various alkaloids – Solanine, Hyoscine, Hyoscyamine

30
Q

nightshade toxicity MOA

A

Solanine inhibits cholinesterase

Hyoscine & Hyoscyamine are similar to atropine - inhibit ACh

31
Q

nightshade toxicity clinical signs

A

anti-sludge (mydriasis, increased heart rate, tremble, apathy, agitated)

GI irritant (colic, hemorrhagic diarrhea)

32
Q

Know the 3 major categories of photosensitization

A

1.Primary
2. Secondary
3. Congenital Defects in Porphyrin Metabolism

33
Q

What are clinical signs of photosensitization?

A

Photophobia, dermatitis, excessive tearing, swelling/redness, increase in sensitivity of non-pigmented skin, ooze serum around lips/eyes/ears/coronary bands of hooves, hair/skin slough in ulcerated areas

34
Q

How do primary photosensitizers cause these clinical signs?

A

Plant is ingested or direct contact with skin
quinones & furanocoumarins are photoreactive → ROS

35
Q

Familiarize yourself with images of the 5 primary photosensitizing plants in powerpoint.

A

St. John’s wort, Buckwheat, Bishop’s weed, Cow Parsnip, Spring Parsley

(Bishop John’s Cow Bucked its skin in the Spring)

36
Q

Define Hepatobiliary or secondary photosensitization.

A

Most common form

diseased liver unable to metabolize phylloerythrin from chlorophyll → photosensitization

37
Q

What toxic alkaloid most commonly causes hepatotoxicity leading to secondary photosensitization?

A

Pyrrolizidine Alkaloids (PA)

38
Q

What is the mechanism of action for this toxin and why does this lead to photosensitization?

A

PA activated by cytochrome P450s in liver; >80% liver damage → PA not conjugated → phylloerythrin accumulation → diseases of the skin

39
Q

What are clinical signs for PA induced toxicity?

A

Liver failure, diarrhea, tenesmus, rectal prolapse, weight loss, neuro signs of hepatic encephalopathy, dermatitis of non-pigmented skin

40
Q

What are diagnostic signs for PA induced toxicity?

A

Liver biopsy, fibrosis, megalocytosis, biliary hyperplasia, elevated liver enzymes, hard fibrotic liver

41
Q

Familiarize yourself with 5 PA containing plants in powerpoint.

A

Senecio spp (Groundsel, Tansy Ragwort), Hounds tongue, heliotrope, fiddle neck rattlepod

(Senna the rattlesnake has PA helical worts on her tongue and neck)

42
Q

How do steroidal sapogenins contribute to secondary photosensitization?

A

Form crystalloid material blocking the biliary system → intrahepatic cholestasis/biliary occlusion

43
Q

What are 4 plants that produce steroidal sapogenins in powerpoint?

A

Agave lechuguilla, bear grass, puncture vine/goat’s head, lantana

44
Q

What congenital conditions could be a differential diagnosis for primary and secondary photosensitization.

A

Congenital Protoporphyria (Aberrant Porphyrin Metabolism Type II)
Bovine Protoporphyria

45
Q

Name plant recently associated with acute hepatotoxicity from contaminated hay

A

Salvia reflexa (lance-leaf sage)

46
Q

Know the mechanism of action of plant induced hemoglobinuria

A

Oxidation of reactive sulfhydryl (S-H) → disulfide bonds → inhibit G6P dehydrogenase → cannot convert NADPH or GSH → oxidant injury to Hb & RBC

47
Q

Why are cats more susceptible to Heinz body formation?

A

Low glucuronyl transferase, slow metabolism, 4x S-H groups in Hb

48
Q

Onion poisoning – toxin

A

n-propyl disulfide

49
Q

Onion poisoning - MOA

A

oxidant injury to Hb and RBC → heinz bodies

50
Q

Onion poisoning - clinical signs

A

hemoglobinuria, weakness/ataxia, anemia/pale mm, tachycardia, onion odor

51
Q

Onion poisoning - treatment

A

remove source
blood transfusions in severely anemic patients
avoid stressing the animal

52
Q

Brassica syndromes – list 5 associated syndromes and treatments, if any.

A
  1. SMCO → hemoglobinuria (treatment: blood transfusion)
  2. Glucosinolates → isothiocyanates/thiocyanates → goiter
  3. Tryptophan → 3-MI → pulmonary emphysema/edema
  4. High sulfur → thiamine & Cu def → polioencephalomalacia (treatment: thiamine)
  5. Hepatotoxicity
53
Q

Brassica treatment

A

blood transfusion for anemia
thiamine for polioenceph
remove source
treat symptoms
corticosteroids for emphysema

54
Q

Brassica induced hemoglobinuria – toxin

A

s-methyl-L-cysteine-sulfoxide (SMCO)

55
Q

Brassica induced hemoglobinuria – MOA

A

SMCO converted to dimethyl sulfide in the rumen → heinz bodies & hemoglobinuri

56
Q

major members of the Brassica family.

A

rape, kale, cabbage, turnips, brussel sprouts

57
Q

Describe how the Descurainia spp. Tansy mustard and Flixweed induce thyroid hyperplasia. Toxin & MOA,

A

Toxin: glucosinolates

MOA: glucosinolates → isothiocyanates/thiocyanates → inhibit iodine uptake by thyroid → no negative feedback resulting increased thyroid hormones → goiter

58
Q

Descurainia spp. Tansy mustard and Flixweed induce thyroid hyperplasia treatment/prevention.

A

treatment: remove from diet, supplement iodine

Prevention: do not feed to pregnant goats

59
Q

Red Maple poisoning – which maples, other trees? Animals effected, Clinical signs

A

Red maple hybrids, silver maple, sugar maple, Pistacia
horses, zebras, alpacas
heinz body anemia, brown/red urine, methemoglobinemia, liver icterus and elevated enzymes

60
Q

red maple leaves poisoning post-mortem findings

A

splenomegaly, hepatomegaly with pale centrilobular areas, brown/black kidney

61
Q

Moldy Sweet Clover toxin and how is it created

A

coumarin
penicillin & aspergillus spp convert coumarin into dicourmarol

62
Q

Moldy Sweet Clover MOA

A

depletes vitamin K clotting factors (prothrombin & factors 7,9,10)

63
Q

Moldy Sweet Clover clinical signs

A

hematomas, hematuria, hemarthrosis, hyphema, abortion, weakness, low PTT

64
Q

Moldy Sweet Clover treatment

A

whole blood transfusion
vitamin K1
(vitamin K3 less effective)