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Toxicology > Hematologic, Respiratory, Metabolic, and Cardio Toxins > Flashcards

Hematologic, Respiratory, Metabolic, and Cardio Toxins Flashcards

1
Q

What is Melilotus spp?

A

Moldy sweetclover

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2
Q

What was isolated from moldy sweetclover?

A

Dicourmarol

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3
Q

What is the most common intoxication in small animals?

A

Anticoagulant rodenticides

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4
Q

What is found in 1st generation anticoagulant rodenticides?

A

Warfaring, pindone, chorophacinone

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5
Q

What is found in 2nd generation and longer anticoagulant rodenticides?

A

Bromadiolone, brodifacoum, diphacinone

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6
Q

What is the anticoagulant MOA?

A

Interferes with the conversion of vitamin K and its 2,3 epoxide
Inhibits carboxylation of coagulation proteins clotting factors 2, 7, 9, 10
Binds with plasma albumin and competes with other protein bound xenobiotics

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7
Q

Where does the metabolism of coumarins occur?

A

Liver

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8
Q

What species is the most susceptible to anticoagulant toxicities?

A

Swine

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9
Q

What are the clinical signs and lesions associated with anticoagulant toxicities?

A 
Hemorrhage
Green or blue-green feces
CNS signs
SQ hematomas
Lameness
Hypovolemic shock
Abortions
Sudden death
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10
Q

What is the clinical pathology with anticoagulant toxicity?

A

Prolongation of any clotting test
PT 1st because of factor 7
By 48 hours, PTT is elevated

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11
Q

What is the treatment for rodenticide toxicity when there are no clinical signs?

A

Decontamination of GI tract: emesis or activated charcoal with cathartic
Vitamin K PO or monito PT

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12
Q

What is the treatment for rodenticide toxicity when there are clinical signs?

A

Correct low PCV, hypovolemia, provide clotting factors

Vitamin K

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13
Q

What is the duration of treatment with warfarin toxicosis?

A

10-14 days

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14
Q

What is the duration of treatment with bromadiolone toxicosis?

A

21 days

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15
Q

What is the duration of treatment with diphacinone, brodifacoum toxicosis?

A

30 days

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16
Q

What are contraindicated drugs during treatment of anticoagulant toxicosis?

A

NSAIDs

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17
Q

What are sources of coumarin anticoagulants?

A

Rodenticides
Moldy sweetclover poisoning
Coumadin

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18
Q

What is the toxic prinicple in Melilotus spp (moldy sweetclover)?

A

Coumarin glycosides converted to dicoumarol by molds

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19
Q

What is the MOA of Melilotus spp (moldy sweetclover)?

A

Competitively inhibits the epoxide reductase that activates vitamin K

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20
Q

What species is affected by Melilotus spp (moldy sweetclover)?

A

Livestock, most often cattle

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21
Q

What time of year does Melilotus spp (moldy sweetclover) toxicosis occur?

A

Winter when fed hay

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22
Q

What are the signs of Melilotus spp (moldy sweetclover) poisoning?

A 
Blood loss
Hematomas
Anemia
Epistaxis
Hemorrhagic diarrhea
Abortion
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23
Q

What is the clinical pathology with Melilotus spp (moldy sweetclover)?

A

Prolonged PT and PTT

Decreased PCV and total protein

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24
Q

What are the lesions with Melilotus spp (moldy sweetclover)?

A

Extensive hemorrhages

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25
Q

What is the treatment for Melilotus spp (moldy sweetclover) toxicosis?

A

Discontinue feeding affected hay
Whole blood transfusions
Vitamine K

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26
Q

What is Pteridium aquilinum?

A

Bracken fern

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27
Q

What is the toxic principle in Pteridium aquilinum (Bracken fern)?

A

Ptaquiloside in cattle

Thiaminase in horses

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28
Q

What is the MOA of Pteridium aquilinum (Bracken fern)?

A

Hematopoietic depression in cattle

Thiamine in GI tract in horses

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29
Q

What is the toxic part of Pteridium aquilinum (Bracken fern)?

A

All, especially young plants and rhizomes

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30
Q

What species are affected by Pteridium aquilinum (Bracken fern)?

A

Cattle, horses

Rarely swine

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31
Q

What is the time frame of Pteridium aquilinum (Bracken fern) toxicosis?

A

1-2 months of consumption

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32
Q

What is the time of year for Pteridium aquilinum (Bracken fern) toxicosis?

A

Late summer, early fall

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33
Q

What are the signs of Pteridium aquilinum (Bracken fern) toxicosis?

A 
Emaciation, lethargy
Incoordination (bracken staggers)
Tremors
Bradycardia
Convulsions
Death 2-10 days after signs
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34
Q

What are the lesions with Pteridium aquilinum (Bracken fern) toxicosis in cattle?

A

Generalized hemorrhage, anemia, aplastic marrow

Urinary bladder: hyperplasia –> neoplasms

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35
Q

What are the lesions with Pteridium aquilinum (Bracken fern) toxicosis in horses?

A

Enteritis
Pericardial hemorrhages
Polioencephalomalacia

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36
Q

What is the method of diagnosing toxicosis from Pteridium aquilinum (Bracken fern) in horses?

A

Assay for thiamine in whole blood

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37
Q

What is the treatment for Pteridium aquilinum (Bracken fern) toxicosis in cattle?

A

Blood transfusions
Antibiotics
D,I-batyl alcohol

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38
Q

What is the treatment for Pteridium aquilinum (Bracken fern) toxicosis in horses?

A

Thiamine HCl for days to weeks

Supportive

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39
Q

What is Acer rubrum?

40
Q

What is the toxic principle of Acer rubrum (red maple)?

A

Gallic and tannic acids

41
Q

What is the MOA of Acer rubrum (red maple)?

A

Hemoglobin oxidant

42
Q

What is the toxic part of Acer rubrum (red maple)?

A

Leaves, especially wilted and dried

43
Q

What are the species affected by Acer rubrum (red maple)?

44
Q

What is the time frame of Acer rubrum (red maple) toxicosis?

A

4-5 days after consumption

45
Q

What is the time of year Acer rubrum (red maple) toxicosis occurs?

A

Mostly July to October

46
Q

What is the toxic dose of Acer rubrum (red maple)?

A

> 1.5 g/kg BW dried red maple leaves

47
Q

What is the sign of acute 1st phase of Acer rubrum (red maple) toxicosis?

A

Methemeglobinemia

48
Q

What is the sign of acute 2nd phase of Acer rubrum (red maple) toxicosis?

A

Heinz body anemia
Icterus* (extravascular)
Hemoglobinemia, hemoglobinuria (intravascular)

49
Q

What is the lab diagnosis of Acer rubrum (red maple) toxicosis?

A

Methemoglobinemia without anemia initially
Heinz bodies
Low PCV
Hyperbilirubinemia

50
Q

What are the lesions with Acer rubrum (red maple) toxicosis?

A

Renal: tubular nephrosis, Hb casts in kidney (if intravascular)
Spleen: erytyrophagocytosis, hemosiderosis (extravascular)

51
Q

What is the treatment of Acer rubrum (red maple) toxicosis?

A 
Ascorbic acid to reduce MetHb to Hb
α-tocopherol less effective
Supportive
Whole blood transfusions
Fluids, diuresis to reduce Hb nephrosis
52
Q

What is the prevention of Acer rubrum (red maple) toxicosis?

A

Don’t plant near horse barns
Remove downed limbs or trees immediately after storms
Prevent accumulation of leaves in pastures or hay

53
Q

What is Allium?

A

Onions, garlic

54
Q

What is the toxic principle of Allium (onions, garlic)?

A

Large variety of sulfur-containing oxidants including N-propyl disulfide
Raw, dried, cooked garlic and onions

55
Q

What is the MOA of Allium (onions, garlic)?

A

Hemolysis of RBCs occurs when oxidative injury from Allium-derived SCOs exceeds erythrocyte antioxidant capabilities
Heinz bodies with hemolysis, secondary to oxidant effect

56
Q

What is the toxic part of Allium (onions, garlic)?

57
Q

What are the species affected by Allium (onions, garlic)?

A

All. Horses and cattle are the most susceptible LA

Dogs, cats most susceptible SA

58
Q

What is the time frame of Allium (onions, garlic) toxicosis?

A

Dose dependent

59
Q

What are the signs of Allium (onions, garlic) toxicosis?

A

Transient gastroenteritis

Acute hemolytic crisis: cyanosis, low PCV, Heinz bodies, hyperbilirubinemia, HBemia/Hburia, icterus

60
Q

What is the treatment of Allium (onions, garlic) toxicosis?

A

Supportive therapy: O2 and/or blood replacement

Cats: no methylene blue –> Hz body anemia and MetHb

61
Q

What can cause acute bovine pulmonary emphysema (ABPE) or acute respiratory disease syndrome (ARDS?

A

Ruminants and horses: 4-ipomeanol
Perilla frutescens
Ruminants only: lush forage, Brassica sp, 3-methylindole

62
Q

What is the toxic principle of perilla mint?

A

Perilla ketone (3-substituted furan)

63
Q

What is the MOA of perilla mint?

A

Mixed function oxidases bioactivate

64
Q

What is the most toxic part of perilla mint?

A

Flowers and seeds

65
Q

What is the toxic principle of lush forage?

66
Q

What is the toxic principle of moldy sweet potato?

A

4-ipomeanol

67
Q

What is the MOA for ABPE/ARDS?

A

Free radicals, lipid peroxidation

68
Q

What are the signs of ABPE/ARDS?

A

Dyspnea, cyanosis, disorientation, bellowing, recumbency, death

69
Q

What are the lesions with ABPE/ARDS?

A

Pulmonary emphysema
Type I cells are absent or necrotic
Type II cells replace type I cells causing a glandular appearance

70
Q

What is the treatment of ABPE/ARDS?

A

Minimize stress

Supportive

71
Q

What is the prevention of ABPE/ARDS?

A

Avoid abrupt dietary change
Limit grazing of Perilla mint during flowering
Limit intake of moldy sweet potatoes
Ionophores and tetracyclines to inhibit growth of Gm+ ruminal bacteria that convert tryptophan to indole

72
Q

What is the MOA of urea toxicosis?

A

NH3 absorbed in bloodstream –> toxic to enzymes in TCA cycle

73
Q

What does causes toxicity with NPN?

A

0.3-1.5 g/kg bw

74
Q

What factors influence toxicity of NPN?

A 
Dose
Adaptation
Acute poisoning
pH of rumen
High energy feeds needed for proper utilization of urea
Death from lactic acidosis or hyperkalemic heart failure
Maturity of animals
Hydration
Hepatic insufficiency
Lack of natural protein
Fasting
Plants with ureases enhance hydrolysis of urea
75
Q

What are the signs of urea toxicosis?

A

Acute onset: 0.5-6 hours
Salivation, abdominal pain
Muscle tremors, hyperthermia, convulsions
Recumbency, bloat, regurgitation of rumen contents

76
Q

What is the lab diagnosis of urea toxicosis?

A

Metabolic acidosis
Blood ammonia: 1-4 mg/dl
Rumen ammonia: >80 mg/dl
Rumen pH >7.5

77
Q

What is the treatment of urea toxicosis?

A

Ruminal infusion of cold water and acetic acid, 6 hour intervals to 48 hours
Treatment for metabolic acidosis
Rumenotomy to remove contaminated feed

78
Q

What are examples of andromedotoxins?

A 
Rhododendron spp (Rhododendron, Azaleas)
Kalmia (Laurel, lambkill, calfkill)
Pieris japonica (Japanese peris)
79
Q

What is the toxic principle of andromedotoxins?

A

Andromedotoxins (diterpenoids)

80
Q

What is the MOA of andromedotoxins?

A

Toxins bind to and keeps Na channels open

Prlonged depolarization and excitation

81
Q

What is the toxic part of andromedotoxins?

A

All, especially leaves and flower nectar

82
Q

What species are affected by andromedotoxins?

A

All, cattle, sheep, goats, horses

83
Q

What is the time frame of andromedotoxins?

A

Acute, usually hours

84
Q

What is the toxic dose of andromedotoxins?

A

1-3% BW in cattle experimentally

85
Q

What are the signs of andromedotoxins?

A

Salivation, burning sensation in mouth. emesis, diarrhea

Bradycardia, hypotension, AV block

86
Q

What is the treatment of andromedotoxins?

A 
Emesis
Supportive therapy:
fluid therapy
Atropine for bradycardia
Isoproterenol for heart block
87
Q

What are Taxus spp. and Cephalotaxus spp?

88
Q

What is the toxic principle of Taxus spp. and Cephalotaxus spp (Yew)?

A

Taxine alkaloids A and B

89
Q

What is the MOA of Taxus spp. and Cephalotaxus spp (Yew)?

A

Inhibits depolarization in the heart

90
Q

What is the toxic part of Taxus spp. and Cephalotaxus spp (Yew)?

A

All except ripe fruit

91
Q

What species are affected by Taxus spp. and Cephalotaxus spp (Yew)?

A

All livestock, dogs, wild animals, humans

Monogastrics are more sensitive

92
Q

What is the time frame for Taxus spp. toxicosis?

A

Acute, sudden death common

93
Q

What is the toxic dose of Taxus spp?

94
Q

What are the signs of Taxus spp. toxicosis?

A

Trembling, muscle weakness, dyspnea, collapse

Arrythmiam, bradycardia, heart block

95
Q

What are the lesions associated with Taxus spp?

96
Q

Where is Taxus spp. consistently found?

97
Q

What is the treatment for Taxus spp?

A 
Remove from source
Respiration
Emesis
Gastric lavage
Activated charcoal and salin cathartic
Atropine early
Maintain body fluid and electrolyte balance

Toxicology (4 decks)

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