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Tox > Final Exam > Flashcards

Final Exam Flashcards

1
Q

Name the 6 different types of acids:

A
  1. Insoluble Ca2+ Oxalates
  2. Soluble Ca2+ Oxalates
  3. Isocupressic acid
  4. Quinones
  5. Tannic Acid
  6. Triterpene acid
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2
Q

Name some insoluble Ca2+ oxalate plants:

A

A. Arum Family

  1. Chinese Evergreen, 2. Elephant’s ear, 3. Flamingo plant, 4. Jack in the pulpit, 5. Cuckoo plant, 6. Caladium, 7. Dumcane, 8. Devil’s Ivy, 9. Swiss cheese plant, 10. Philodendron, 11. Peace lily , 12. Skink cabbage, 13. Arrowhead vine, 14. Calla lily

B. Aralia Family

  1. Umbrella tree

C. Palm Family

  1. Fishtail palm
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3
Q

Dumcane causes _________ release.

A

Histamine

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4
Q

Which parts of insoluble Ca2+ oxalate plants are toxic?

A

All parts!

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5
Q

Name some soluble Ca2+ oxalate plants:

A
  1. Halogeton, 2. Greasewood, 3. Pigweed
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6
Q

Soluble Ca2+ oxalate plants primarily cause what?

A

Hypocalcemia and kidney damage.

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7
Q

Name a isocupressic acid plant?

A

Ponderosa pine

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8
Q

Isocupressic acid mainly causes what?

A

Vasoconstriction and abortion.

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9
Q

Name a quinone plant.

A

St. John’s Wort.

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10
Q

Quinones primarily cause what?

A

Primary photosensitization

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11
Q

Name a tannic acid plant.

A

Oak tree

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12
Q

Tannic acid plants mainly cause what?

A

Tissue damage including GI lesions and kidney damage.

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13
Q

Name some triterpene acid plants:

A
  1. Lantana and 2. Yellow Sage
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14
Q

Triterpene acid plants mainly cause what?

A

Liver damange and hepatogenic photosensitization.

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15
Q

Name the 13 different types of alkaloids:

A
  1. Colchicine
  2. Diterpene
  3. Ergot
  4. Indolizidine
  5. Lycorine
  6. Muscarine
  7. Piperidine
  8. Pyridine
  9. Pyrrolizidine
  10. Solanine/Solanidine
  11. Taxine
  12. Tropane (Atropine, Hyoscine, Hyoscyamine)
  13. Xanthine (Caffeine, Theobromine, Theophylline)

**Basically ANYTHING that ends in -ine, except ergot!!**

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16
Q

Name some colchicine plants:

A
  1. Autumn crocus
  2. Glory lily
  3. Meadow Saffron
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17
Q

Colchicine plants mainly cause what?

A

They are antimitotic by binding to tubulin and inhibiting spindle formation during cell division.

Rapidly dividing cells are the most sensitive.

Whole body effected.

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18
Q

Name some Diterpene plants:

A
  1. Buttercup
  2. Larkspur
  3. Monkshood, Aconite
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19
Q

Diterpene plants mainly cause what?

A

Competitive blockade of nicotinic receptors at the muscle endplate similar to curare.

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20
Q

What would you use to treat Diterpene toxicity?

A

Physostigmine or Neostigmine

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21
Q

Monkshood and Aconite cause mostly what?

A

Cardiotoxicity

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22
Q

What is an example of an ergot plant?

A

Ergot is not a plant it’s a fungus and it typically infects plants like rye, and other cereals.

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23
Q

Ergot typically causes what signs?

A

Vasoconstriction, and gangrene

Uterine contractions (abortion)

Acute CNS signs

Chronic signs are more common– Hoof and hair abnormalities.

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24
Q

Name some Indolizidine plants:

A
  1. Locoweeds
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25
Q

Indolizidine typically cause what signs?

A

They inhibit lysosomal enzymes essential for formation of glycoproteins.

Also inhibit neurotoxic alkaloids.

Neurotoxic signs

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26
Q

Name an example of a Lycorine plant:

A

Amaryllis

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27
Q

Lycorine plants typically cause what?

A

Vomiting and diarrhea

and other severe GI signs

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28
Q

Which part of a Lycorine plant is the most toxic?

A

The bulb

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29
Q

Name a Muscarine plant:

A

Poisonous mushroom

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30
Q

What do Muscarine plants cause?

A

CNS stimulation

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31
Q

What are some examples of Piperidine plants:

A
  1. Hemlock
  2. Lupinus
  3. Tobacco
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32
Q

What are some examples of Piperidine plant signs?

A

NM stimulation

NM blockage

Mainly ataxia

Birth defects–skeletal malformations and cleft palates

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33
Q

What are the Pyridine plants:

A

Nightshade family (nicotine and lobaline)

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34
Q

What do Pyridine plants cause?

A

They act on nicotinic receptors at autonomic ganglia, NM junctions and CNS.

Rapid onset of clinical signs- DEATH~from respiratory failure.

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35
Q

What are some examples of Pyrrolizidine plants:

A

Senecio

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36
Q

What are the effects of Pyrrolizidine?

A

Hepatotoxicity

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37
Q

Name some Solanine/Solanidine plants:

A

Black nightshade

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38
Q

What are the effects of Solanine/Solanidine plants?

A

GI, CNS, Respiratory and Cardiac signs

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39
Q

Name some Taxine plants:

A

Japanese Yew*

[has been asked on previous exams]

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40
Q

What are the effects of Taxine plants?

A

Cardiotoxic and GI signs

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41
Q

Name some Tropane (Atropine, Hyoscine, Hyoscyamine) plants:

A
  1. Jimsonweed
  2. Devil’s trumpet
  3. Angel’s trumpet
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42
Q

Name some Xanthine (Caffeine, Theophylline, Theobromine) plants:

A
  1. Cocoa
  2. Coffee arabica
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43
Q

What are the effects of Xanthine plants?

A

Blocking adenosine receptors

Inhibiting phosphodiesterase

Tachycardia and hypotension, salivation, V/D, colic, CNS stimulation (seizures), muscle tremors and urination.

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44
Q

Name the 13 different types of glycosides:

A
  1. Anthraquinone
  2. Calcinogenic (Vit D Analogs)
  3. Carboxyatractyloside (sulfated glycosides)
  4. Cardiac glycosides
  5. Coumarin
  6. Cyanogenic
  7. Cycasin
  8. Glucosinolate (Thiocyanate)
  9. Nitropropanol
  10. Phytoestrogens
  11. Protoanemonin
  12. Ptaquiloside
  13. Steroidal Saponins
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45
Q

Name a type of Anthraquinone plant:

A

Coffee weed, senna

Aloe

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46
Q

What are the effects of Anthraquinone plants?

A

Skeletal and cardiac muscle degeneration

Severe diarrhea

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47
Q

Name some Calcinogenic (Vitamin D Analog) plants:

A

Day Blooming Jessamine

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48
Q

What are the effects of Calcinogenic plants?

A

Hypercalcemia

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49
Q

Name some Carboxyatractyloside plants:

A

Cocklebur

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50
Q

What are the effects of Carboxyatractylosides?

A

Hepatotoxicity

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51
Q

Name some cardiac glycosides:

A
  1. Foxglove
  2. Oleander
  3. Milkweed
  4. Lily of the valley
  5. Christmas kallanchoe
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52
Q

What are the effects of cardiac glycosides?

A

Cardiotoxicity--they inhibit Na+/K+ ATPase

Severe GI irritation

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53
Q

What are some Coumarin plants?

A

Sweet clover

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54
Q

What are the effects of Coumarin plants?

A

Hemorrhage

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55
Q

What are some cyanogenic plants?

A

Wild cherries

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56
Q

What are the effects of cyanogenic plants?

A

Stressed or damaged plants release HCN.

Causes histotoxic anoxia (acute)

Neuronal degeneration (chronic)

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57
Q

Name some cycasin plants:

A
  1. Cycad palm
  2. Sago palm
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58
Q

What are the effects of cycasin plants?

A

GI irritation and liver damage.

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59
Q

Cycad palms have how many toxins, and what does each one cause?

A

3 total:

  1. Cycasin: GI irritation, liver damage
  2. BMAA- neurotoxic
  3. Unk- axonal degeneration in the CNS
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60
Q

Name some Glucosinolate (thiocyanate) plants:

A
  1. Brassica
  2. Soybean
  3. Flax
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61
Q

What are the effects of glucosinolate plants?

A

SCN- antithyroid

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62
Q

Name some nitropropanol plants:

A

Milkvetch

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63
Q

What are the effects of nitropropanol plants?

A

Inhibits enzymes of the Citric Acid cycle

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64
Q

Name some Phytoestrogen plants:

A

Alfalfa

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65
Q

What are the effects of phytoestrogen plants?

A

Infertility

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66
Q

Name some Protoanemonin plants:

A

Buttercup family

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67
Q

What are the effects of Protoanemonin plants?

A

Severe irritation of the GI tract

and dermatitis.

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68
Q

Name some Ptaquiloside plants:

A

Bracken fern

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69
Q

What are the effects of some ptaquiloside plants?

A

Aplastic anemia- in cattle and sheep

Neoplasia of the urinary tract causing enzootic bovine hematuria.

Tumors of the upper GI tract and retinal degeneration in sheep (bright blindness)

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70
Q

Name some Steroidal Saponins:

A

Agave

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71
Q

What are the effects of Steroidal Saponins?

A

Liver damage and

hepatogenic photosensitization

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72
Q

Name the 9 different types of proteins and amino acids:

A
  1. Dimethyl Sulfide
  2. Propyl Disulfide
  3. Diterpene Esters
  4. Grayanotoxins
  5. Lectins (Phytotoxins, toxalbumins)
  6. Meliatoxins
  7. Tetradymol
  8. Thiaminase
  9. Titerpenoid Saponins
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73
Q

Name the Dimethyl Disulfide plants:

A

Mustards

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74
Q

What are the effects of Dimethyl Disulfide plants?

A

Heinz bodies and Hemolytic anemia

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75
Q

Name some Propyl Disulfide plants:

A
  1. Onion
  2. Garlic
  3. Shallots
  4. Chives
  5. Leak
  6. Allium
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76
Q

What are the effects of propyl disulfide plants?

A

Heinz bodies and hemolytic anemia

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77
Q

Name some Diterpene esters:

A
  1. Cat tail
  2. Croton
  3. Poinsettia
  4. Manchineel
  5. Wild physicnut
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78
Q

What are the effects of Diterpene Esters?

A

Irritation and blistering of the skin and GI mucosa.

Especially horses

Enzyme dysfunction–direct cell injury

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79
Q

Name some Lectins (Phytotoxins) plants:

A
  1. Castor bean
  2. Precatory bean
  3. Beans (soybeans, kidney, pinto, navy)
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80
Q

What are the effects of Lectin plants?

A

Hemorrhagic gastroenteritis

One castor bean can kill a small child

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81
Q

Name some Meliatoxin plants:

A

Chinaberry

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82
Q

What are the effects of Meliatoxin plants?

A

Enterotoxicity

Neurotoxicity

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83
Q

Name some Tetradymol plants:

A

Horsebrush

Sagebrush

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84
Q

What are the effects of Tetradymol plants?

A

Hepatogenic photosensitization- SHEEP

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85
Q

Name some Thiaminase plants:

A
  1. Horsetail
  2. Brackenfern
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86
Q

What are the effects of Thiaminase plants?

A

Signs of thiamine (Vitamin B1) deficiency–neurotoxic.

Commonly affects piglets.

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87
Q

Name some Titerpenoid Saponin plants:

A
  1. Alfalfa
  2. Holly
  3. English ivy
  4. Pokeweed
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88
Q

What are the effects of Titerpenoid Saponin plants?

A

Direct irritation of the GI mucosa.

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89
Q

Name the different types of unclassified toxins:

A
  1. Red clover
  2. Avocado
  3. Black walnut
  4. Forage-induced photosensitzation
  5. Grapes and Raisins
  6. Lily
  7. Pigweed
  8. Red Maple
  9. Senna
  10. Yellow Starthistle
  11. Macademia nuts
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90
Q

What is the MOA of Red Clover?

A

Hepatotoxicity and 2ndary photosensitization

Mainly effects horses.

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91
Q

Avocado can cause sudden death in these species:

A

Goats, horses, rabbits and caged birds.

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92
Q

Black walnut have been known to cause what?

A

Laminitis in horses

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93
Q

What 2 plants can cause forage induced photosensitization?

A

Moldy alfalfa and red clover

~either primary or secondary photosensitization

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94
Q

Grapes and raisens cause what?

A

Renal failure in dogs

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95
Q

Lillies (like Easter lily and Day lily) cause what?

A

Nephrotoxicity in cats

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96
Q

Pigweed contains 3 toxins which are:

A
  1. Nitrate- causes methemoglobinemia
  2. Oxalate- hypocalcemia and kidney damage
  3. Unknown- Renal tubular nephrosis in ruminats, pigs and horses
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97
Q

Dried Red Maple leaves cause what?

A

Hemolytic anemia

Hemoglobinemia

and Heinz bodies

in horses.

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98
Q

Coffee senna causes what?

A

An unknown myotoxin causes skeletal muscle myopathy and cardiomyopathy.

Anthraquinone glycoside acts as a cathartic, can cause V/D.

Diarrhea

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99
Q

Yellow Starthistle causes what?

A

Nigropalladial encephalomalacia (ENE)

Chewing disease

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100
Q

Macademia nuts cause what?

A

Hind limb weakness

Depression

Ataxia

Tremors

Hyperthermia

Lameness

Recumbency

V/D

Colic

Pale mm

Full recovery within 2 days

Signs are seen in DOGS

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101
Q

Name some Resins or Resinoids:

A
  1. Milkweeds
  2. Marijuana
  3. Chinaberry
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102
Q

Resins or resinoids cause what?

A

Irritation of the nervous or muscle tissue

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103
Q

Name a Gossypol plant:

A

Cottonseed

104
Q

What are the effects of Gossypol plants?

A

Cardiotoxicity and secondary liver damage

Reduces male fertility by destroying seminiforous tubules.

105
Q

What are some minerals we should be concerned with that cause toxicity?

A
  1. Molybdenum
  2. Copper
  3. Selenium
  4. Nitrate
106
Q

I say Halogeten you say….

A

Soluble oxalate, causes hypocalcemia

107
Q

I say Oak tree you say….

A

Tannic acid, causes tissue damage.

108
Q

I say Ponderosa Pine you say….

A

Isocupressic acid, causes vasoconstriction and abortion.

109
Q

I say Dumcane you say…

A

Insoluble oxalate, causes histamine release

110
Q

I say Yellow Sage you say….

A

Triterpene acid, hepatogenic photosensitization

111
Q

I say St. John’s Wort you say…

A

Quinones, Primary photosensitzation.

112
Q

I say Locoweeds you say…

A

Indolizidine, neuro signs.

113
Q

I say Japanese Yew, you say….

A

Taxine

114
Q

I say Nightshade family you say…

A

Pyridine, act on nicotinic receptors in the autonomic ganglia.

115
Q

I say Senecio you say….

A

Pyrrolizidine, hepatotoxicity

116
Q

I say tobacco you say…

A

Piperidine

117
Q

I say poisonous mushroom you say…

A

Muscarine

118
Q

I say Amaryllis family you say…

A

Lycorine

119
Q

I say buttercup, you say…

A

Diterpene

120
Q

I say cocoa you say…

A

Xanthine, inhibits phosphodiesterase

121
Q

I say Devil’s trumpet you say…

A

Tropane

122
Q

I say Monkshood you say….

A

Diterpene

123
Q

I say Meadow Saffron you say….

A

Colchicine

124
Q

I say black nightshade you say…

A

Solanine/Solanidine

125
Q

I say Coffee weed you say…

A

Anthraquinone,

126
Q

I say Buttercup family you say….

A

Protoanemonin

127
Q

I say wild cherries you say…

A

Cyanogenic, release of HCN

128
Q

I say agave you say….

A

Steroidal saponins

129
Q

I say Milkvetch you say…

A

Nitropropanol, inhibits the citric acid cycle.

130
Q

I say sweet clover you say…

A

Coumarin

131
Q

I say Oleander you say….

A

Cardiac glycoside

132
Q

I say sago palm you say….

A

Cycasin (even though this is only 1 of 3 toxins, the other is BMAA and the other is unk)

133
Q

I say cocklebur you say…

A

Carboxyatractyloside

134
Q

I say Day-Blooming Jessamine you say…

A

Calcinogenic

135
Q

I say bracken fern you say….

A

Ptaquiloside

136
Q

I say alfalfa you say….

A

Phytoestrogens

137
Q

I say Brassica you say…

A

Glucosinolate

138
Q

I say Castor bean you say…

A

Lectin (phytotoxin)

139
Q

I say Holly you say…

A

Titerpenoid saponins

140
Q

I say Horsebrush you say…

A

Tetradymol

141
Q

I say Rhododendron you say….

A

Grayanotoxins

142
Q

I say onion you say…

A

Propyl disulfide, causes heinz bodies and hemolytic anemia.

143
Q

I say mustards you say…

A

Dimethyl Disulfide, causes Heinz bodies and Hemolytic anemia.

144
Q

I say croton you say…

A

Diterpene esters causes irritation to the skin and GI mucosa, specifically horses.

145
Q

I say Chinaberry you say…

A

Meliatoxin

146
Q

Ponderosa Pine/Isocupressic acid is an:

A. Acid

B. Alkaloid

C. Glycoside

D. Protein and amino acid

E. Unclassified Toxin

A

Acid

147
Q

Oleander is an:

A. Acid.

B. Alkaloid

C. Glycoside

D. Protein and amino acid

E. Unclassified Toxin

A

Glycoside

148
Q

Pigweed is an:

A. Acid

B. Alkaloid

C. Glycoside

D. Protein and amino acid

E. Unclassified toxin

A

Unclassified toxin

149
Q

Sweet clover/Coumarin is an:

A. Acid

B. Alkaloid

C. Glycoside

D. Protein and amino acid

E. Unclassified toxin

A

Glycoside

150
Q

Ergot is an:

A. Acid

B. Alkaloid

C. Glycoside

D. Protein and amino acid

E. Unclassified toxin

A

Alkaloid

151
Q

Castor bean/Lectin is an:

A. Acid

B. Alkaloid

C. Glycoside

D. Protein and amino acid

E. Unclassified toxin

A

Protein and amino acid

152
Q

Name some plants that accumulate Nitrate/Nitrite:

A
  1. Pigweed
  2. Oats
  3. Alfalfa
  4. Wheat
  5. Sweet Clover
  6. Corn
  7. Johnson/Sudan Grass
153
Q

What is the MOA of Nitrate/Nitrite?

A

Nitrate + reductase >> Nitrite >> Enters RBCs and converts ferrous to ferric

>> Methemoglobinemia>> Anoxia

154
Q

What does Nitrate/Nitrite cause?

A

Vasodilation>>hypotension

Abortion

Tachypnea, restlessness, dyspnea, weakness, ataxia, recumbency, cyanosis, terminal convulsions and death.

155
Q

How would you diagnose Nitrate/Nitrite poisoning?

A

Test the forage, hay or water.

Test brown blood for a ratio of blood: phosphate buffer 1:2

Diphenylamine test

Post-Mortem test: Ocular fluid

156
Q

How would you treat Nitrate/Nitrite poisoning?

A

Methylene Blue 1% slowly IV

do NOT use in cats!!!

Activated charcoal, gastric lavage with cold water.

Antibiotics

Animals sadly usually die before treatment!!!

157
Q

What is the most toxic portion of a Nitrate rich plant?

A

Stalk>Leaves>Seeds

158
Q

T/F: Older mature plants are higher in Nitrate.

A

False, young plants usually are.

159
Q

_______ are the most susceptible to Nitrate

______ are the most sensitive to Nitrite IV

_______ are resistant to Nitrate.

A

Cattle most susceptible

Horses most sensitive

Pigs are resistant.

160
Q

T/F: Young animals are the most sensitive to Nitrate/Nitrite poisoning.

A

True

161
Q

T/F: Anemia and methemoglobinema increase the toxicity of Nitrate/Nitrite.

A

True

162
Q

What plants tend to accumulate cyanide?

A
  1. Wild cherries
  2. Sudan grass, Johnson grass, sorghum
  3. Lima bean and cassava roots (tapioca)
  4. Apples, plums, apricots
163
Q

What is the acute MOA of cyanide?

A

Blocks electron transport and causes histotoxic anoxia esp to the brain.

Metabolic acidosis

May inhibit glycolysis and citric acid cycle.

164
Q

What is the chronic MOA of cyanide?

A

Neuronal degeneration and demyelination of SC and brain, goitrogenic (disrupts the production of thyroid hormones).

165
Q

What are the acute effects of cyanide toxicity?

A

Vasoconstriction and irritation of the mucous membranes.

Bright red mucous membranes

Tachypnea, gasping, salivation, tremors, lacrimation, urination, defecation, colic, vomiting, clonic convulsions, death.

166
Q

How do you diagnose cyanide toxicity?

A

The smell of cyanide in blood.

Preserve samples with mercuric chloride in urine.

Lactic acidosis>>increased anion gap.

Sodium pricate test.

Post-mortem can test brain and heart tissue.

167
Q

What are the chronic effects of cyanide toxicity?

A

Posterior paralysis

Urinary incontinence

Constipation

Cystitis

Goitrogenic (disrupts the production of thyroid hormones)

168
Q

How would you treat cyanide toxicosis?

A

Sodium nitrite IV>>this will lead to methemoglobinemia>> Binds cyanide + reactivates cytochrome oxidase.

So you are basically treating a toxin with another toxin!

Sodium thiosulfate

Oxygen

Vinegar + Cold Water slows microflora

Mineral oil (to act as a laxative)

169
Q

Which animals are most susceptible to cyanide poisoning?

A

Ruminants

(Cattle>Sheep)

170
Q

T/F: The smell of cyanide resembles bitter almond or ammonia.

A

True

171
Q

What is the most toxic part of a plant that accumulates cyanide?

A

Seeds>Leaves>Bark>Stems>Fruit

172
Q

T/F: Older plants or those with less N or P may have deceased levels of glycosides.

A

False, Younger plants and those with increased levels of N or P will have inc. glycosides.

173
Q

What are some plants that accumulate soluble oxalate?

A
  1. Pigweed
  2. Beets
  3. Lamb’s Quarters
  4. Sorrel, Soursop
  5. Rhubarb
  6. Greasewood
174
Q

Other than plants, what are some other places soluble oxalates may be found?

A

Household and industrial products

Fungi

Ethylene glycol

175
Q

What is the MOA of soluble oxalate?

A

Combines with Ca2+ and forms insoluble Ca2+ oxalate.

Causes hypocalcemia and tetany.

This effects bone and milk production.

Precipitates in the kidney tubules and causes damage and necrosis.

176
Q

What are the clinical signs of soluble oxalate toxicity?

A

Dull, Depressed, Twitching, Weak, Head and neck pulled to one side, Prostration, Coma, Death

Tachypnea, Blood tinged froth, Convulsions, Fatal renal tubular toxicosis–oliguria, depression, hyperkalemia and cardiac failure.

Chronic tubular nephrosis.

177
Q

How do you diagnose soluble oxalate toxicity?

A

Demonstrate Ca2+ oxalate (polarizing rosette) in kidney tubules, kidney will be dark

red with a gray line.

Hypocalcemia

Increased BUN (azotemia)

178
Q

How do you treat soluble oxalate toxicity?

A

Treatment is of little value after clinical signs emerge.

Activated charcoal and limewater.

Ca2+ gluconate IV- not curative.

Saline glucose (alkalosis and diuresis)

Ca2+ supplement and high Ca2+ diet is protective.

Supportive therapy for nephrosis.

179
Q

Which species are most susceptible to soluble oxalate toxicosis?

A

Ruminants (sheep and cattle)

180
Q

What is the most toxic part of the plant for those that accumulate soluble oxalate?

A

Leaves>Seeds>Stems

181
Q

______ reduces the rate of absorption of soluble oxalate.

A

Food

182
Q

_____ decreases the toxicity of soluble oxalate.

A

Calcium

183
Q

What is the MOA of Ammonia?

A

It is a strong irritant of the mucous membranes.

There is an increased chance of 2ndary resp infections.

Lung congestion due to increased permeability.

Respiratory alkalosis with compensatory metabolic acidosis.

May inhibit the citric acid cycle.

184
Q

What are the clinical signs of ammonia toxicosis?

A

Red mucous membranes

Lacrimation

Nasal discharge

Coughing/sneezing/dyspnea

Decreased growth and egg production in birds

Cyanosis

CNS stimulation: clonic convulsions

185
Q

How do you diagnose ammonia toxicitiy?

A

Ammonia odor

There is no chemical analysis for toxic gases

186
Q

How do you treat ammonia toxicosis?

A

Removal of the source

Proper ventilation

Fresh air

Ointment for the eyes

Antibiotics

Diuretics

187
Q

What is a common source of ammonia?

A

Decomposing manure in animal houses.

188
Q

What animals are most susceptible to ammonia toxicosis?

A

Livestock

189
Q

What is the MOA of Hydrogen Sufide?

A

In lower concentrations: irritation of ocular, respiratory mucosa and lungs.

In large concentrations: sudden collapse, cyanosis, dyspnea, anoxic convulsions, rapid death.

190
Q

Describe hydrogen sulfide gas:

A

Colorless, flammable, and has a rotten egg odor.

191
Q

How would you diagnose Hydrogen Sulfide gas toxicity?

A

Dark or greenish-purple tissues.

The blood is dark and may not clot.

Sewage smell.

GI contents may be black or dark and smell like sewage.

192
Q

How would you treat Hydrogen sulfide toxicity?

A

Remove the souce.

Give Sodium nitrate IV + Cyanide>>Methemoglobinemia>>Binds Hydrogen Sulfide + Reactive Cytochrome Oxidase

Oxygen and Supportive Therapy

193
Q

How is Hydrogen sulfide gas produced?

A

By decomposition of urine and feces.

194
Q

T/F: Hydrogen sulfide is the most dangerous sewage gas.

A

True

195
Q

T/F: Exposure to 4 ppm of Hydrogen Sulfide is quickly fatal.

A

False, exposure to 400 ppm is rapidly fatal.

196
Q

T/F: Hydrogen sulfide reacts with silver, iron, lead and other metals to form dark/black compounds.

A

True

197
Q

What is the MOA of Carbon Monoxide?

A

Combines with Hb (hemoglobin)>>CarboxyHb>>Can’t carry O2 + interferes with O2 release from Hb anoxemia>>Death.

198
Q

What are the clinical signs of Carbon Monoxide poisoning?

A

Sudden death

Hypoxia

Ataxia

Dyspnea

Lethargy

Coma

Bright red blood with healthy pink mucous membranes

Chronically: Brain edema, hemorrhage, deafness

199
Q

How do you diagnose Carbon Monoxide poisoning?

A

Measure [CO] in the air.

Measure % COHb in whole blood (refridgerate)!!!

200
Q

What are the characteristics of Carbon Monixide?

A

Colorless and Odorless

201
Q

How would you treat Carbon Monixide poisoning?

A

O2 or 5% CO2 in O2 (to displace CO from Hb)

Blood transfusion

202
Q

What is the MOA of Nitrogen Oxide?

A

Increased chance of 2ndary respiratory infections.

Irritation of the mucous membranes (nitric acid).

May cross respiratory mucousa and cause cellular damage.

Lung damage.

Death by anoxemia.

203
Q

What are the clinical signs of Nitrogen Oxide toxicosis?

A

Pulmonary edema

Hemorrhage

Emphysema

Bronchiolitis with granulation tissue

Methemoglobinemia

Cyanosis

Necrosis of skeletal muscle.

204
Q

How would you diagnose Nitrogen Oxide toxicosis?

A

History

205
Q

What is the treatmet for Nitrogen oxide toxicosis?

A

Fresh air, oxygen

Diuretics

Antioxidants (Actetylcysteine, Vitamin E)

Methylene Blue IV

206
Q

How is nitrogen oxide formed?

A

From incomplete reduction of nitrates during fermentation in silos.

DO NOT enter if there is an irritant odor or yellow haze.

207
Q

NO2 has a _______ color,

while N2O4 is ________.

A

N2O has a red-brown color while

N2O4 is colorless.

208
Q

What is the MOA of Sulfur Oxide gas?

A

Sharply irritant to mucous membranes (sulfurous and sulfuric acid).

Can get reflex bradycardia.

Lung damage and death by anoxemia.

209
Q

What are the clinical signs of Sulfur Oxide gas?

A

Odor causes choking, coughing and suffocation.

210
Q

How would you diagnose Sulfur Oxide toxicosis?

A

Similar to other gases.

211
Q

How would you treat sulfur oxide toxicosis?

A

Supportive care

212
Q

Bufo toad toxins are found in the _________ toad on the east coast and

the __________ toad in the southwestern region.

A

Cane/Marine

Colorado River

213
Q

Cane toads are found in which states or areas?

A

FL, southern TX, Hawaii, Puerto Rico

214
Q

Colorado River Toads are found in what area?

A

Southwestern US from Arizona to CA.

215
Q

The toxins are found in what glands of the toad?

A

Parotid salivary

216
Q

What are the toxins within the toads?

A

Catecholamines, Serotonin

Bufagenins and Bufotoxins= cardioactive steroids

Indole alkylamines= similar to LSD (hallucinogenic)

217
Q

What is the MOA of the Bufo Toad Toxin?

A

Irritation of the mucous membranes.

Effects the heart, blood vessels and CNS.

It is Digitalis-like and so it inhibits the Na+/K+ ATPase pump.

Causes vasoconstriction and hallucination

218
Q

What are the clinical signs of the Bufo Toad Toxin?

A

Irritation–hypersalivation/foaming, brick red mucous membranes, vocalization, vomiting.

Neurologic signs–disoriented, ataxia, circling, seizures, opisthotonus, hyperthermia, coma

Cardiovascular signs– tachypnea, tachycardia, arrhythmias, bradycardia and collapse.

219
Q

How would you diagnose Bufo Toad Toxin?

A

Digoxin may be elevated

There would be a moderate incresae in hemoglobin, PCV, BG, BUN, ALP, K+, Ca2+, Ph

220
Q

How would you treat Bufo Toad Toxin?

A

Flush the mouth and use activated charcoal.

Digoxin immune Fab.

Symptomatic seizure control.

Atropine for most things but contraindicated if tachypnea!!

221
Q

What types of snakes are classified as pit vipers?

A

Rattlesnakes

Copperheads

Cottonmouths

Water mocasins

*Their head is broad and triangular and they have rectangular fangs in the upper jaw.*

222
Q

Where are pit vipers found?

A

Every state except Maine, Alaska, and Hawaii.

223
Q

Describe Pit Viper toxins:

A

Enzymatic and nonenzymatic proteins and amino acids: “killing fraction”

224
Q

Which species are most sensitive and susceptible to pit viper bites?

A

Dogs

225
Q

Which pit viper snake has the most toxic bite?

A

Rattlesnakes

226
Q

What is the MOA of Pit Viper bites?

A

Hyaluronidase causes venom to spread.

Phospholipase A2 disrupts cell membranes, uncouples, phosphorylation and releases vasoactive enzymes.

Enzymatic/nonenzymatic proteins= hematoxic –> procoagulant, anticoagulant, cardiotoxic and neurotoxic.

227
Q

What are the clinical signs of a pit viper bite?

A

Can be rapid or delayed by several hours.

Local tissue reactions: puncture wounds, fang marks, bleeding, edema, swelling, eccymosis, petechiation, necrosis.

228
Q

How would you diagnose a pit viper bite?

A

Echinocytosis, hemolysis, hemoconcentration, increased OR decreased coagulation time, DIC.

Hypo or Hyperkalemia, liver and renal failure.

229
Q

How would you treat a pit viper bite?

A

Keep calm and keep the bite wound below the level of the heart.

Polyvalent cortalid antivenom (available for dogs and may cause allergic rxns)

Diphenhydramine IV/SC

Supportive care

Fentanyl Patch

Immobilization of animal

Corticosteroids, NSAIDs- are NOT RECOMMENDED.

Rattlesnake vaccine for dogs but antivenom still recommended.

230
Q

What is the MOA of a Coral Snake bite?

A

Local tissue reaction- due to hyaluronidase, proteinase, ribonuclease, deosuribonuclease, and phospholipase.

Neurotoxic

Non depolarizing neuromuscular blockage (curare-like)

231
Q

60% of coral snake bites are what?

A

Non-envenomating (they have a poor delivery of toxin)

232
Q

What are the clinical signs of a Coral Snake bite?

A

Local signs: puncture wounds

Cats/Dogs: CNS depression, quadriplegia w/decreased spinal reflexes, respiratory paralysis, hypotension, and v-tach.

Dogs only= intravascular hemolysis, anemia, hemoglobinuria, maybe vomiting and excessive salivation.

Cats= do NOT show hemolysis, anemia, hemoglobinura.

Aspiration pneumonia is an important complication.

233
Q

How would you diagnose a Coral Snake bite?

A

Elevated fibrinogen and creatine kinase.

Morphologic changes to the surface of the RBC, anemia and hemoglobinuria.

Aspiration pneumonia may be visible on radiographs.

234
Q

How would you treat a coral snake bite?

A

Specific Micrurus fulvius antivenom.

Supportive care

235
Q

What is the MOA of Amphetamines?

A

CNS stimulant, block reuptake of norepinephrine and dopamine.

Inhibits MAO.

Exact mechanism is still unknown.

Peripherally- sympathomimetic effect by releasing norepinephrine and direct stim on alpha-adrenergic receptors and B-adrenergic receptors

236
Q

What are the toxokinetics of Amphetamines?

A

pH dependent urinary excretion

237
Q

What are amphetamines typically used for?

A

ADHD treatment

Narcolepsy

etc…

238
Q

What are the clinical signs of amphetamine toxicosis?

A

Hyperactivity, restlessness, circling, tremors, ataxia, seizures, mydriasis, hypersalivation, hyperthermia.

Some may show depression, weakness and bradycardia.

239
Q

How would you diagnose amphetamine toxicosis?

A

Hypoglycemia; tremors may result in metabolic acidosis and rhabdomyolysis.

May be able to detect amphetamines in blood, urine and saliva.

240
Q

How would you treat amphetamine toxicosis?

A

Induce emesis, repeated activated charcoal for sustained release.

Benzodiazepines are NOT recommended.

Urinary acidfiers will enhance urinary excretion as long as patient is not acidodic.

Symptomatic or supportive care.

241
Q

Cocaine is an ______ from the leaves of the plant Erythroxylum coca or E. monogynum from Mexico, South America, Indonesia and the West Indies.

A

Alkaloid

242
Q

Which animals are most sensitive and susceptible to cocaine toxicity?

A

Dogs

243
Q

Cocaine is absorbed from…

A

All mucous membranes, crosses the BBB and alveolar capillaries.

244
Q

What is the MOA of cocaine?

A

CNS stimulant and sympathomimetic; blocks reuptake of NE/Dopamine/Serotonin.

Increases catecholamine release; sensitizes sympathetic effector cells to catecholamines.

Direct effect on myocardium.

245
Q

What are the clinical signs of cocaine toxicosis?

A

Vomiting, hypersalivation, mydriasis, hyperactivity, tremors, convulsive seizures, hyperthermia, tachycardia, tachypnea.

246
Q

What are the lesions associated with cocaine toxicosis?

A

Myocardial degeneration, subendocardial and epicardial hemorrhage, pericardial effusion, pulmonary hemorrhage.

247
Q

How would you diagnose cocaine toxicosis?

A

Elevated CK, systemic acidosis.

Can detect in serum, plasma, urine and stomach contents.

248
Q

How would you treat cocaine toxicosis?

A

Induce vomiting if no clinical signs- may precipitate seizures.

Gastric lavage with activated charcoal.

Monitor the body temperature.

Symptomatic/supportive treatment

249
Q

What is the name of the marijuana plant?

A

Cannabis sativa

250
Q

What are the properties of Cannabis?

A

THC and several other Cannabinoids

251
Q

There is 10% THC in _______.

20% THC in _________.

5% THC in________.

A

10% THC in hashish (dried resin from flower tops).

20% THC in hasish oil.

5% THC in sinsemilla= seedless marijuana

252
Q

What is the toxicokinetics of marijuana?

A

THC is highly lipid soluble; oral absorption is INCREASED by a fatty meal.

Binds extensively to plasma proteins (up to 99%)

Metabolized to several active metabolites; one of which is more potentent than THC and crosses the BBB.

Enterohepatic recirculation.

253
Q

What is the MOA of Marijuana?

A

2 cannabinoid receptors ID’d

CB1- widely distributed in the brain (alters activity of neurotransmitters) and effects on memory, perception and control of movement.

Both CB1 and CB2 are immune cells.

254
Q

What are the clinical signs of Marijuana toxicosis?

A

Vomiting, CNS depression, ataxia, incoordination, tremors, weakness, mydriasis, and hypothermia.

255
Q

How would you diagnose Marijuana toxicosis?

A

Can be detected in urine and stomach contents.

Mainly based on history and clinical signs.

Human urine tests are not effective in dogs.

256
Q

How would you treat Marijuana toxicosis?

A

Usually resolves spontaneously without treatment.

Emesis (but not usually effective b/c THC is an anti-emetic.)

Repeated activated charcoal.

Symptomatic, monitor the body temperature.

Recovery may take a few days.

Wide safety margin and unlikely to be fatal.

Tox (3 decks)

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