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Toxicology-soph-c > Tox-3 > Flashcards

Tox-3 Flashcards

1
Q

Which form of arsenic is more toxic?

A

Inorganic arsenic

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2
Q

Which form of arsenic is highly associated with CNS effects?

A

Pentavalent

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3
Q

Which form of arsenic is associated with blood and CV effects?

A

Trivalent

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4
Q

Where is pentavalent arsenic metabolized?

A

Reduced and metabolized in the rumen

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5
Q

How is trivalent arsenic metabolized?

A

Binds to -SH groups, disrupting cell metabolism and inhibits oxidative phosphorylation

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6
Q

What clinical signs are associated with an arsenic toxicosis?

A

Intense abdominal pain, gastroenteritis, vomiting, weakness, staggering gait, PU/PD progressing to oliguria and anuria, dehydration, thirst

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7
Q

What differentials must you consider when observing the blood-related clinical signs of arsenic?

A

Ergot

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8
Q

What blood-related clinical signs are expected with arsenic toxicity?

A

Cold extremities due to poor perfusion and subnormal temperature

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9
Q

What CNS related clinical signs are expected with arsenic toxicity?

A

Salivation, trembling, depression, and posterior paresis

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10
Q

What characteristic lesion in the abomasum is associated with arsenic toxicity?

A

Brick red gut

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11
Q

Which toxin must you consider whenever there is sudden onset of GI or sudden death, especially dead animals found in or near water?

A

Arsenic

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12
Q

How do you treat arsenic toxicity?

A

GI decontamination (only if acute!), chelation therapy, supportive therapy (demulcents, fluids)

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13
Q

What is the classic chelating antidote for arsenic toxicosis?

A

Dimercaprol (complete with -SH groups for available arsenic)

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14
Q

What can you use for chelation therapy for arsenic toxicosis before displaying clinical signs?

A

Sodium thiosulfate

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15
Q

What is the prognosis for arsenic toxicosis?

A

Guarded to poor

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16
Q

Pennies made before what year are 96% zinc?

A

1982

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17
Q

What is the mechanism of action of zinc toxicosis?

A

Free zinc is released in the stomach’s acidic environment forming zinc salts leading to corrosive effect to stomach and intestinal mucosa; oxidative damage

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18
Q

What are the “big three” clinical signs of zinc toxicity seen in both acute and chronic toxicity?

A

GI tract bleeding, renal failure, and hemolysis

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19
Q

How do you diagnose zinc toxicosis?

A

Serum zinc levels >10ppm, regenerative anemia, thrombocytopenia, elevated liver, kidney, and pancreatic enzymes, hemoglobinuria

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20
Q

Is emesis indicated in zinc toxicosis?

A

Yes! As quickly as possible if the animal hasn’t already vomited (unless an exploded battery)

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21
Q

How do you treat zinc toxicosis?

A

Remove foreign body, symptomatic (fluids, blood products), proton-pump inhibitors (omeprazole) or H2 blockers

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22
Q

At what pH are you worried about the caustic effects and damage to the GI tract?

A

High (alkaline) pH

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23
Q

What clinical signs do you expect with soap/shampoo toxicosis?

A

GI distress

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24
Q

How do you treat soap/shampoo toxicosis?

A

Dilution with milk or water

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25
Q

What type of necrosis does scouring powder/bleach cause?

A

Liquefactive necrosis

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26
Q

What are the clinical signs of scouring powder/bleach toxicosis?

A

Vomiting, drooling, and abdominal pain

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27
Q

What is the gold standard treatment for scouring powder/bleach toxicosis?

A

Milk or water, gastrointestinal protectants

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28
Q

Is emesis or lavage contraindicated in scouring powder/bleach toxicosis?

A

Yes! Caustic

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29
Q

What is the mechanism of action of phenols?

A

Denatures and precipitates cellular proteins thus destroying all contacted cells

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30
Q

What are the clinical signs of phenol toxicosis?

A

Corrosive burns of oral-esophageal pathway, vomiting, hypersalivation, ataxia, panting -> shock, cardiac, arrhythmias, methemoglobinemia, hepatic and renal damage, coma

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31
Q

How are pine oils detoxified?

A

Glucuronidation (cats more susceptible to toxicosis!)

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32
Q

What are the clinical signs of pine oils?

A

Nausea, hypersalivation, blood vomit, abdominal pain, ataxia, hypotension, respiratory depression, acute renal failure, pulmonary edema

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33
Q

What are the clinical signs of automatic dishwasher detergents toxicosis?

A

Vomiting, diarrhea, salivation, GI pain, and oral, esophageal, gastric erosions

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34
Q

How do you treat automatic dishwasher detergents toxicosis?

A

Dilution with milk or water, analgesics and possibly steroids for inflammation

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35
Q

What is the pH of toilet bowl cleaner?

A

Low pH (acidic)

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36
Q

What mycotoxin is a metabolite of Fusarium spp. That is a reproductive toxicant?

A

Zearalenone

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37
Q

What makes zearalenone hard to get rid of in the environment?

A

Heat stable and resistant to most mold retardants (even if the fungus is killed, the toxin is still active)

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38
Q

Which species are resistant to zearalenone toxicosis?

A

Chickens

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39
Q

What is the mechanism of action of zearalenone?

A

Estrogen receptor agonist

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40
Q

What syndrome does zearalenone toxicosis cause?

A

“Hyperestrogen” syndrome - vulvovaginitis and estrogenic responses

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41
Q

How do you diagnose zearalenone toxicosis?

A

Presence of toxin in feed

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42
Q

What is the difference between venomous and poisonous animals?

A

Venomous animals actively inject toxins and poisonous animals secrete poisons which are passive defense mechanisms

43
Q

What three classes of compounds comprise venom?

A

LMW substances (PG, histamine, epi), peptides/proteins (direct toxic effects), enzymes (cause toxicity and allergy)

44
Q

What is the difference between bee and wasp/hornet stings?

A

Bees can only sting one, wasps/hornets sting repeatedly

45
Q

What is the mechanism of action of bee venom?

A

Mellitin causes pain and histamine release, phospholipase A2 destroys membranes

46
Q

What is the mechanism of action of wasp/hornet venom?

A

Some contain neurotoxins, kinins induce pain

47
Q

What is the mechanism of action of ant venom?

A

Piperidine causes dermal necrosis and formic acid causes burning sensation and pain

48
Q

What are the clinical signs of bee, wasp, hornet venom toxicosis?

A

Swelling, redness, and edema at the site, anaphylaxis, systemic toxicity

49
Q

How do you treat bee, wasp, hornet, fire ant venom toxicity?

A

Scrape retained stinger to remove, cold compress, antihistamines and corticosteroids, monitor for anaphylactic reactions (Epi, IV fluids PRN)

50
Q

What two species of ticks are venomous?

A

Dermacentor and Ixodes

51
Q

What is the toxin produced in the salivary glands of ticks?

A

Holocyclotoxin

52
Q

What is the mechanism of action of holocyclotoxin?

A

Impairs acetylcholine release at neuromuscular junction (results in weakness and paralysis)

53
Q

What other mechanism of action is associated with Dermacentor toxin?

A

Acts on Na+ channels

54
Q

After how long after attachment of a tick do you observe clinical signs?

A

6-14 days

55
Q

What are the clinical signs of holocyclotoxin toxicosis?

A

Loss of appetite and voice, incoordination, ascending flaccid paralysis, excessive salivating and vomiting, respiratory distress, death due to respiratory paralysis

56
Q

How do you diagnose holocyclotoxin toxicosis?

A

No definitive diagnosis! History or presence of ticks

57
Q

What are the 2 major clinical signs that suggest holocyclotoxin toxicosis?

A

Ascending paralysis and loss of voice

58
Q

What medication can be used to reverse the mechanism of action of holocyclotoxin toxicosis?

A

Atropine sulfate

59
Q

What is the prognosis of holocyclotoxin toxicosis?

A

Good if treated

60
Q

Which species of Bufo toad is found in Florida?

A

B. Marinus

61
Q

What is the mechanism of action of toad poisoning?

A

Secretions from the toad include biogenic amines (histamines) and Bufogenins (bufotalin)

62
Q

What is the mechanism of action of bufogenins (bufotalin)?

A

Inhibit sodium-potassium ATPase; produce toxic cardiac arrhythmias

63
Q

What should you differentiate from when suspecting Bufo toad toxicosis?

A

Cardiac glycoside producing plant toxicosis

64
Q

What clinical signs can be present in Bufo toad toxicosis?

A

Hypersalivation and/or foaming at the mouth; head, shaking, vomiting; hyperemic gums; arrhythmias; neurological signs (convulsions, ataxia, hallucinations)

65
Q

What electrolyte abnormality is present with Bufo toad toxicosis?

A

Severe hyperkalemia

66
Q

What treatment is indicated in Bufo toad toxicosis?

A

GI and oral decontamination, seizure control, antiarrhythmics, fluid replacement therapy, digoxin-specific antigen-binding fragments

67
Q

How do you treat the severe neurologic signs/hyperkalemia associated with Bufo toad toxicosis?

A

Digoxin-specific antigen-binding fragments (may be cost prohibitive)

68
Q

What toxin does the venom from female black widow spiders contain?

A

Alpha-latrotoxin

69
Q

What is the mechanism of action of alpha-latrotoxin?

A

Creates pores in membranes allowing Ca++ entry and releasing massive amounts of neurotransmitter -> sustained muscle spasms

70
Q

What clinical signs are associated with black widow spider venom toxicosis?

A

Muscle cramping and spasms, rapid weight loss, abdominal rigidity, restlessness, writhing, vocalization, hypertension, tachycardia, respiratory collapse

71
Q

Which species is most sensitive to the venom of black widow spiders?

A

Cats

72
Q

How do you treat alpha-latrotoxin toxicosis?

A

Control muscle spasms and pain (methocarbamol), anti-venom, supportive care

73
Q

What is the only proven treatment for alpha-latrotoxin toxicosis?

A

Anti-venom

74
Q

What enzyme is present in the venom from brown recluse spiders that binds to cell membranes and cleaves heads off lipids?

A

Sphingomyelinase D

75
Q

What determines the severity of the lesion caused by the brown recluse venom?

A

Victim’s immune response

76
Q

What are the clinical signs of brown recluse envenomation?

A

Redness, swelling, tenderness, bulls eye non healing ulcer; hemolytic anemia, fever, weakness, leukocytosis

77
Q

How do you diagnosis brown recluse envenomation?

A

Difficult if bite isn’t witnessed

78
Q

How do you treat brown recluse envenomation?

A

Dapsone, fluids, anti-inflammatories, glucocorticoids, antibiotics, analgesics

79
Q

All venomous snakes are members of the which two families?

A

Elapidae or Crotalidae

80
Q

What determines the severity of the clinical signs observed with a venomous snake bite?

A

Size of victim and amount of venom delivered (as well as age of snake!)

81
Q

What causes victims of venomous snake bites to die?

A

Respiratory paralysis

82
Q

What is the mechanism of action of the venom from an Eastern Coral Snake?

A

Bungarotoxin is neurotoxic that prevents binding of ACh causing paralysis

83
Q

What are the clinical signs of Eastern Coral Snake envenomation?

A

Salivation, dyspnea, weakness, hyporeflexia, CNS depression, paralysis, myoglobinemia in cats and hemolysis in dogs

84
Q

What diagnostic test is used to diagnose Eastern Coral Snake envenomation?

A

No definitive diagnostic tests

85
Q

Is there an anti-venom for Eastern Coral Snake envenomation?

A

Yes - administer if neurologic signs develop

86
Q

How do you treat Eastern Coral Snake envenomation?

A

Anti-venom, ventilatory support, antibiotics and symptomatic wound care, monitoring for >/= 24 hours

87
Q

What is the prognosis of Eastern Coral Snake envenomation?

A

Good

88
Q

What pit vipers are part of the Crotalid family?

A

Copperhead,cottonmouth, rattlesnakes

89
Q

What are the clinical signs of Crotalid (pit viper) envenomation?

A

Fang marks, swelling and bruising at site of bite, pain, hypotension, shock, tachycardia, tachypnea, anticoagulation, tissue necrosis

90
Q

What is the only proven therapy for Crotalid (pit viper) envenomation?

A

Anti-venom

91
Q

What is the mechanism of action of enterotoxins from garbage and carrion toxicity?

A

Bind to intestinal epithelium, increasing permeability and causing fluid loss (diarrhea) and decreased absorption of nutrients

92
Q

What are the clinical signs of entertoxins from garbage/carrion toxicity?

A

Vomiting, diarrhea, abdominal pain, stasis with gas accumulation and bowel distension

93
Q

What is the source of endotoxins in garbage/carrion?

A

LPS from gram negative cell walls

94
Q

What are the clinical signs of endotoxins from garbage/carrion toxicity?

A

Lethargy, fever followed by hypothermia, diarrhea, abdominal pain, shock, extremely bad smelling feces

95
Q

How do you treat endotoxin toxicity from garbage/carrion?

A

Emesis, support CV function, correct fluid and electrolyte imbalances, antibiotics

96
Q

What is considered to be the most potent toxin on Earth?

A

Clostridium botulinum toxin

97
Q

What is the mechanism of action of botulinum toxin?

A

Prevents release of ACh at neuromuscular junction causing paralysis

98
Q

How do you diagnosis clostridium botulinum toxicosis?

A

Very difficult! Only circumstantial evidence (access to carrion, garbage, compost piles)

99
Q

What are the clinical signs of clostridium botulinum toxicosis?

A

Decreased tongue and tail tone, dropping food from mouth, salivation, weakness, weak vocalization, progressive paresis, bradycardia, constipation, urinary retention

100
Q

What other differential diagnoses must be considered when suspecting clostridium botulinum toxicosis?

A

Anticholinesterases, ionophores, lead, and nitrate poisoning

101
Q

Is there an antitoxin for clostridium botulinum toxin?

A

Yes!

102
Q

What is the prognosis of clostridium botulinum toxin toxicosis?

A

Poor

103
Q

How do you treat clostridium botulinum toxin toxicosis?

A

Supportive therapy, IV fluids, respiratory support, O2 therapy, warm water enemas and bladder expression if necessary, antibiotics, and antitoxin

Toxicology-soph-c (4 decks)

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