Plant 2 Primary photosenstizer, Hemolysis, Hemostasis

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69 Terms

1
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Hypericum perforatum

St. Johnswort, Klamath weed, goatweed

<p><strong>St. Johnswort</strong>, Klamath weed, goatweed </p>
2
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True or False? St. Johnswort is a very common weed throughout the PNW so it often causes issues

False. St. Johnswort is a very common weed throughout the PNW.but it RARELY causes issues becuase it not very palatable

3
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What is the toxic principle and MoA of Hypericum perforatum?

primary photodynamic pigment, hypericin, reaches cutaenous circulation where reacts with oxygen and sunlight to cause inflammation

<p>primary photodynamic pigment, hypericin, reaches cutaenous circulation where reacts with oxygen and sunlight to cause inflammation </p>
4
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Hypericum perforatum toxicosis occurs at ___% of BW requiring a little/a lot of plant material.

1-5%, requires a lot of plant material

5
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What animals are affected by Hypericum perforatum?

any grazing animal

6
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What lesions are seen with Hypericum perforatum toxicity?

lesions restricted to nonpigmented areas, including cornea and conjunctiva with varying degrees of inflammation within 24 hours of ingestion

7
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How do you treat and control Hypericum perforatum toxicity?

avoid plant and keep animals out of sunlight

abx, anti-inflammatories like corticosteroids, warm soaks

8
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In humans, hyperforin from Hypericum perforatum is a potent inhibitor of ___,___,___,____, and can interfere with over __ drug metabolism/excretion.

serotonin, dopamine, noradrenaline, GABA (no more effective than placebo for treatment of moderate-severe major depression)

50

9
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What are examples of Allium spp.

onions, garlic, chives, scallions, leeks, shallots, etc

<p>onions, garlic, chives, scallions, leeks, shallots, etc</p>
10
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What plant can be confused with wild allium species?

death camas

11
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There are both ___ and ___ varities of allium species

cultivated, wild

12
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What are the toxic principles in allium spp.? Where do you find them?

disulfides, sulfoxides, highest concentration in bulb

13
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Disfulfides and sulfoxides are ____ ____ agents so can cause what type of anemia?

potent oxidizing,

Heinz body hemolytic anemia

14
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__probably have twice the risk for oxidant injury with allium spp. vs. what species?

cats, dogs

15
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What is the rule of thumb regarding how toxic an allium form is?

the stronger the smell, the more toxic

16
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True or False? Onions are 3-5x more toxic than garlic.

False. Garlic is 3-5x more toxic than onions

17
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True or False? Dried onion and garlic products are much more concentrated and toxic compared to fresh.

True

18
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There is a large range of toxic doses for onions because it depends on ___.

form: cooked, fresh, dried are all a risk

19
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What animals are most sensitive and most resistant to allium spp.?

Most sensitive: cattle, cats

Most resistant: sheep, goats, humans

20
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The onset of clinical signs is faster with onions/garlic?

The onset of clinical signs is faster with onions (garlic is slower)

21
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What are some clinical signs of allium spp. toxicity?

acute onset within few days, peak at 3-5 days

icterus, dyspnea, weakness, collapse, abortions due to hypoxia in cows

22
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What lab abnormalities are seen with allium spp.?

Heinz body formation (within 24-48h)

Hemolysis (within 3-5d), anemia, hemoglobinemia/uria, methemoglobinemia, jaundice

23
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What secondary changes are seen on necropsy with allium spp.?

hemoglobinuric (hypoxic) nephrosis, centrilobular necrosis

24
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With allium spp. exposures in companion animals, what and when should you be monitoring?

PCV and blood smear at baseline, day 2-3, day 5 (garlic may require longer monitoring)

25
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What is the treatment for allium spp.?

remove source, DO MATH, bathe, emesis, AC, monitor CBC, IV or SQ fluids, transfusion if hemolysis

26
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What is the prognosis for allium spp.?

Good, if not moribund

27
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__can tolerate onions at 100% of diet for periods of time, with transient effects. There are recommendations on how much can go into __ feed

sheep, ruminant

28
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Acer spp.

maple

<p>maple </p>
29
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What is the toxic principle in Acer spp.?

Unknown - wilted or dried senescent leaves or bark often the culprit and suspected gallic acid, tannic acid, pyrogallol

30
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True or False? Red maple Acer rubrum is the only species to cause toxicosis

False. Consider all Acer spp. species potentially a problem.

<p>False. Consider all <em>Acer spp. </em>species potentially a problem.</p>
31
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What species does Acer spp. affect?

equine (reported in zebra, donkey), report in 2 alpacas, other species potentially susceptible

<p>equine (reported in zebra, donkey), report in 2 alpacas, other species potentially susceptible</p>
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What is the MoA of Acer spp.?

acute hemolytic anemia, metheomglobinemia, Heinz body formation

33
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What clinical signs and clinical pathology do you see with Acer spp.?

within 24 hours: lethargy, anorexia, tachycardia, tachypnea, brown discoloration to blood, red tinted serum

anemia, methemoglobinemia, hemoglobinuric nephrosis

<p>within 24 hours: lethargy, anorexia, tachycardia, tachypnea, brown discoloration to blood, red tinted serum</p><p>anemia, methemoglobinemia, hemoglobinuric nephrosis</p>
34
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What is the treatment for Acer spp.?

same for most hemolytic anemias

35
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What 2 Acer spp species is associated with Seasonal Pasture Myopathy (acute rhabdomyolysis) in equids?

Box elder (Acer negundo), Sycamore maple (Acer pseudoplatanus)

36
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How do equids get Seasonal Pasture Myopathy?

ingesting tree fruit and seedlings of Box elder or sycamore maple, which contains hypoglycin A and methylenecyclopropyl-glycine which inhibits enzymes causing selective multifocal monophasic hyaline degeneration of type I muscle fibers

37
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Cruciferae family

mustards! over 300 plants

<p>mustards! over 300 plants</p>
38
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Animals have to eat ___ of Cruciferae to have problems.

A LOT

39
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The toxic principles and MoA varies with __ and __ __ of cruciferae family.

plant, plant part

40
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List the 6 toxic principles within the cruciferae family

  1. goitrin and thiocyanate

  2. thiaminase-like activity, high sulfur

  3. S-methyl cysteine sulfoxide converted to dimethyl disulfide

  4. equine dysmaturity syndrome

  5. GI irritants

  6. atypical pulmonary emphysema/edema (fog fever), nitrate accumulation

41
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What does goitrin and thiocyante do?

interferes with thyroid hormone synthesis and iodine uptake leading to goiter

42
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What does thiaminase like activity or high sulfur do?

causes polioencephalomalacia and secondary copper deficiencies

43
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What does S-methyl cysteine sulfoxide converted to dimethyl disulfide do?

Hemolysis, Heinz body anemia, many others!!

44
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What is Equine dysmaturity syndrome?

congenital hypothyroidism leading to prolonged gestation, hyperplastic thyroids though normal in size, incomplete ossification of carpal and tarsal bones, forelimb and hindlimb contracture, flexural and angular deformities, common digital extensor tendon ruptures, mandibular prognathism

<p>congenital hypothyroidism leading to prolonged gestation, hyperplastic thyroids though normal in size, incomplete ossification of carpal and tarsal bones, forelimb and hindlimb contracture, flexural and angular deformities, common digital extensor tendon ruptures, mandibular prognathism</p>
45
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Grazing intake of Brassica should not be greater than __% for dairy cows, __% for beef cattle, and lambs can consume up to __%

33%, 70%, 100%

46
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What clincial sign does GI irritants from cruciferae cause?

bloat

47
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True or False? Cruciferae plants can cause BALD (brassica induced liver disesae), which can lead to primary photosensitivity (Type 1)

False. Cruciferae plants can cause BALD (brassica induced liver disease), which can lead to secondary photosensitivity (Type 3 due to reduction of phylloerythrin excretion, accounts for 68.5% of all photosensitivity cases)

48
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What animals are affected by cruciferae?

All species susceptible, mostly seen reports in equids

49
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Describe the clinical signs seen with cruciferae toxicity

  1. enlarged thyroids, young born weak and die shortly after birth

  2. lethargy, incoordination, muscle tremors, blindness, recumbency, convulsinos, death within 2-10 days with copper deficiency

  3. jaundice, hemoglobinemia/uria, anemia, hemolysis, anorexia, feer, Heinz body formation

50
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Describe the lesions seen with cruciferae toxicity

swollen pale liver, jaundice, dark/red brown kidneys, splenomegaly, hepatic and renal hemosiderosis and degeneration/necrosis

51
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What are the treatment options for each toxic principle in cruciferae?

  1. goiter → supplement with iodine

  2. thiaminase like activity → thiamine hydrochloride, mannitol, dexamethason, Cu supplement

  3. hemoslysis → symptomatic and supportive

  4. -6. EDS, bloat, fog fever → symptomatic and supportive, methylene blue for nitrate problems

52
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Melilotus spp.

sweet clover

<p>sweet clover </p>
53
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Melilotus spp. is primarily a __ problem and was aka __.

Historical, moldy sweet clover disease

54
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What is the toxic principle of Melilotus spp?

Coumarin dimerized and oxidzed to dicoumarol during curing process if feed is put of wet, mold is responsible for this conversion

55
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What is the MoA of Melilotus spp?

Dicoumarol interferes with vitamin K epoxide reductase, interferes with activation of clotting factors 2,7,9,10 resulting in bleeding disorders

56
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What animals are affected by Melilotus spp?

primarily cattle

57
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What clinical signs and clinical pathology do you see with Melilotus spp?

varies depending on where bleeding is occurring, anemia and prolonged clotting times

58
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What lesions do you see with Melilotus spp?

generalized hemorrhage

59
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What is the treatment for Melilotus spp?

supportive via vitamin K1, fluids, blood transfusions, alflalfa etc

60
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Pteridium aquilinum

bracken fern

<p>bracken fern</p>
61
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What is the toxic principle of Pteridium aquilinum?

ALL parts toxic

young plants (fronds, croziers) and rhizomes most toxic (green or dried), most toxicosis occur with contaminant of hay

62
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<p>What animals does <em>Pteridium aquilinum</em> affect?</p>

What animals does Pteridium aquilinum affect?

monogastrics (horses), ruminants (cattle, sheep)

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In ___, a diet composed of __% of bracken fern for 3 or more weeks is associated with a __

monogastrics (horses), 20-25%, neurotoxicosis (type 1 thiaminase) or polioencephalomalacia-like disease

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Ruminant diseases from Pteridium aquilinum is due to what?

ptaquiloside (water soluble)

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In ___ , large amounts of braken fern ingested over several ___, leads to ____. This is most common in ___.

ruminants, weeks, bone marrow depression (affecting PLT, WBC, RBCs)

North America

<p>ruminants, weeks, bone marrow depression (affecting PLT, WBC, RBCs) </p><p>North America</p>
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Small daily long term ingestion of braken fern leads to ____ and other ___.

enzootic hematuria, neoplasms

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Long term exposure of braken fern in sheep has led to ____.

retinal degeneration “bright blindness” glassy eyed appearance, dilated pupils

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What clinical signs are seen in monogastrics vs ruminants vs sheep with Pteridium aquilinum?

monogastrics: polioencephalomalacia like disease (acute onset, weight loss, bradycardia, death in 2-10d)

ruminants: bone marrow depression leading to weakness, generalized hemorrhage

sheep: atrophy of outer nuclear layer and rod/cone layer

<p><u>monogastrics</u>: polioencephalomalacia like disease (acute onset, weight loss, bradycardia, death in 2-10d)</p><p>r<u>uminants</u>: bone marrow depression leading to weakness, generalized hemorrhage</p><p><u>sheep</u>: atrophy of outer nuclear layer and rod/cone layer</p>
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What is the treatment for Pteridium aquilinum?

thamine hydrochloride in monogastrics,

abx and supportive care in ruminants