Unit 2 - Venoms and Poisons II Flashcards

1
Q

Are male or female black widow spiders associated with envenomation?

A

females

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2
Q

What do female black widow spiders look like?

A

Shiny black with red or orange hourglass mark on the ventral abdomen

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3
Q

T/F: Juvenile black widow spiders have different patterns from adults.

A

True

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4
Q

What species are sensitive to black widow spider envenomation?

A

Camels, horses, cats, and dogs

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5
Q

In what species is mortality commonly associated with black widow spider envenomation?

A

Cats

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6
Q

T/F: A single bite from a black widow spider can deliver a lethal dose.

A

True

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7
Q

What are the problematic components in black widow spider venom?

A

Alpha-latrotoxin, other neuroactive proteins, and proteolytic enzymes

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8
Q

What does alpha-latrotoxin do?

A

It is a neurotoxin which binds presynaptically creating a stable Ca pore - this results in increased presynaptic vesicle trafficking and release of neurotransmitters (NE and ACh)

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9
Q

When do black widow spider clinical signs typically manifest?

A

In the first 8 hours post-envenomation

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10
Q

What clinical signs are associated with black widow spider envenomation?

A

Muscle fasciculation, severe abdominal pain may occur, ataxia, and flaccid paralysis

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11
Q

How are black widow spider envenomations treated?

A

Antivenon
Ca gluconate for muscle fasiculations
Narcotics or benzos
Limit IV fluids if hypertensive

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12
Q

What is the prognosis for black widow spider envenomations?

A

Generally good

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13
Q

What does a brown recluse spider look like?

A

Violin-shaped pattern on cephalothorax with the neck of the fiddle extending caudally

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14
Q

When do brown recluse spider bites typically occur?

A

When the spider becomes trapped in undisturbed clothing or bedding

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15
Q

What does brown recluse venom contain?

A

Sphingomyelinase D and hyaluronidase

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16
Q

What does sphingomyelinase D do?

A

Damages plasma membranes of endothelia, erythrocytes, and platelets
Neutrophil recruitment
Reduction in expression of epidermal growth factor

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17
Q

What clinical signs are associated with brown recluse spider envenomation?

A

Local pain and stinging followed by pruritus and soreness
Targetoid lesion
Occasional hemolytic anemia with hemoglobinuria
Systemic loxoscelism with DIC

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18
Q

What does the targetoid lesion caused by brown recluse spiders look like?

A

An ischemic area with a dark central eschar and erythematous background

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19
Q

How is brown recluse spider envenomation treated?

A

Routine wound care, supportive care, and surgical debridement of necrotic lesions

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20
Q

What does the scorpion toxin do?

A

It is neurotoxic and leads to depolarization of the neuromuscular junction

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21
Q

What is a good way to detect if a scorpion is in a room?

A

Use UV light - scorpions will fluoresce bright cyan-green

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22
Q

What clinical signs are associated with scorpion envenomation?

A

Sharp local pain
Tachycardia
Hyperactivity, trashing, writing

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23
Q

What treatment is recommended for scorpion toxicosis?

A

Supportive

Antivenom

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24
Q

What may individual stings from hymenoptera result in?

A

Immediate hypersensitivity reaction/anaphylaxis

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25
Q

How can hymenoptera cause death in non-allergic animals?

A

Via massive envenomation - > 20 stings

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26
Q

What is the main component of bee and wasp venoms?

A

Protein that acts as allergens

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27
Q

What is fire ant venom composed of? Why are they problematic?

A

Alkaloids - cytotoxic, hemolytic, fungicidal, bactericidal, and insecticidal properties

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28
Q

What are the four possible reactions to hymenoptera stings?

A

Local, regional systemic/anaphylaxis, delayed-type hypersensitity

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29
Q

What clinical signs are associated with hymenoptera stings?

A

Edema, erythema, pain at the site of the sting, regional response is an extension of local, anaphylaxis

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30
Q

How are local or regional hymenoptera stings treated?

A

Antihistamines, ice or cool compresses, topical corticosteroid lotions

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31
Q

How are anaphylactic hymenoptera stings treated?

A

Epinephrine
IV crystalloid fluids to prevent shock
Antihistamines, corticosteroids as indicated

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32
Q

What toad species are associated with serious clinical signs following oral exposure?

A

B. marinus and B. alvarius

33
Q

What toxic principle do toads have?

A

Bufotoxins

34
Q

What do bufotoxins contain?

A

Bufogenins and bufotenins

35
Q

Where are bufogenins secreted from?

A

Parotid glands

36
Q

What is the MOA of bufogenins?

A

They are digitalis-like cardioactive compounds that bind to Na/K ATPase pump and alter heart rate and rhythm

37
Q

What do bufotenines do?

A

Vasoactive and neuroactive agents

38
Q

What clinical effects does toad poisoning cause?

A

Immediate salivation, headshaking, and hyperemic mucous membranes
Acute onset of neurologic signs - convulsions, ataxia, nystagmus, and stupor
Trembling, tachypnea, abnormal cardiac rate, and arrhythmias

39
Q

How is toad poisoning treated?

A

On-the-spot decontamination

Emetics if the whole toad is consumed and only ptyalism is observed

40
Q

How is toad posioning treated when there are advanced clinical sings?

A

Sedatives/anticonvulsants to control neuro signs
Cardiac support
Fluids and other supportive therapy as indicated

41
Q

What is the toxic principle of blister beetles?

A

Cantharidin

42
Q

Where is cantharidin contained?

A

In hemolymph and repro glands

43
Q

What does cantharidin do?

A

Induces erosions and ulcers on all mucous membranes

Mycoardial necrosis

44
Q

What is the MOA of cantharidin?

A

It induces the release of serine proteases which causes disintegration of desmosomes which leads to acantholysis

45
Q

How does blister beetle toxin get ingested?

A

With hay - they are trapped in hay during harvest and the crimping process releases the toxin

46
Q

What species is most commonly affected by blister beetles?

A

Horses

It has been reported in cattle and sheep

47
Q

T/F: Blister beetle toxin decreases over time with storage.

A

False - it does not decrease with storage

48
Q

What clinical signs are associated with blister beetle poisoning?

A

Dose depenent: colic, polyuria, hematuria, lesions in oral, GI and urogenital mucosae, dehydration, and shock

49
Q

What clin path abnormalities are associated with blister beetle poisoning?

A

Hypocalcemia and hypomagnesemia

50
Q

What lesions are associated with blister beetle poisoning?

A

Sloughing of gastric and other mucosae
Hyperemic mucous membranes - stomach, intestine, renal pelvis, ureters, and bladder
Myocardial necrosis

51
Q

How are blister beetle poisonings diagnosed?

A

History, observation of beetles in hay, ID of cantharidin

52
Q

In what biologic samples can cantharidin be found in?

A

Urine, GI contents

53
Q

How is blister beetle poisoning treated?

A

Symptomatic - fluids for shock, dehydration
Mineral oil
Analgesics
Remove all suspect feedstuffs

54
Q

How is blister beetle poisoning prevented?

A

Use first cutting hay
Scout for beetles
Control grasshoppers and crickets

55
Q

Most mushroom poisonings occur as a result of ingestion of ______ mushrooms.

A

wild

56
Q

During what time of year does mushroom poisoning typically occur?

A

Fall

57
Q

What clinical signs are associated with hallucinogenic mushroom poisoning?

A
Vomiting, diarrhea
Panting, dyspnea
Muscle spasms
Collapse
Cyanosis
Death
58
Q

How is hallucinogenic mushroom poisoning diagnosed?

A

History of exposure

Observation of mushroom parts in vomitus

59
Q

T/F: The Amanita/Galerina group of mushrooms are composed of the most lethal poisons known.

A

True

60
Q

What toxins do the Amanita/Galerina group of mushrooms create?

A

Phallotoxins

Amatoxins

61
Q

Why are amatoxins so bad?

A

They are highly active, rapidly absorbed
Resistant to stomach acid
Thermostable

62
Q

What is the MOA of the Amanita mushrooms?

A

Amatoxins interfere with RNA polymerase which results in decreased mRNA and protein synthesis

63
Q

What body systems are affected by Amanita mushroom poisonings?

A

The liver, kidneys, and intestine

64
Q

What clinical effect does Amanita mushroom toxicosis?

A

Acute hepatic failure +/- hepatoencephalopathy and coma

65
Q

What are the 4 phases of Amanita mushroom poisoning?

A
  1. Initial latent period
  2. Gastroenteric phase
  3. Second latent period
  4. Organ failure phase
66
Q

How long does the 1st phase of Amanita mushroom poisoning last?

A

6-24 horus

67
Q

What occurs during the 2nd phase of Amanita mushroom poisoning?

A

Sudden sharp colicky abdominal pains
Nausea, vomiting, and watery diarrhea
Stools with blood and mucous shreds

68
Q

What occurs during the 3rd phase of Amanita mushroom poisoning?

A

Apparent recovery - ‘false hope’

69
Q

When does the 4th phase of Amanita mushroom poisoning occur?

A

36-84 hours post exposure

70
Q

What occurs during the 4th phase of Amanita mushroom poisoning?

A

Fulminant hepatic, renal, and multiorgan failure

71
Q

What laboratory results are associated with Amanita mushroom poisoning?

A

Albuminuria, hematuria
Elevated liver enzymes, and serum bilirubin
Rapid decrease in coag factors
Hypoglycemia

72
Q

How is Amanita mushroom poisoning diagnosed?

A

History of exposure

Detection of amanitin by LC-MS

73
Q

What is the ideal antemortem sample for Amanita mushroom poisoning diagnosis?

A

Urine

Serum can be used

74
Q

What is the ideal post mortem sample for Amanita mushroom poisoning?

A

Fresh kidney and/or liver

75
Q

What is the toxic principle of Cortinarius mushrooms?

A

Orellanine

76
Q

What is poisoning by Cortinarius mushrooms often characterized by?

A

Severe oliguric renal failure

77
Q

How is Cortinarius mushroo toxicosis diagnosed?

A

Detection of orellanine in renal biopsies by LC-MS/MS

78
Q

Why should you treat the patient not the mushroom?

A

Many mushrooms contain several toxins in varying concentrations
Toxic or non-toxic mushrooms grow side by side so mixed exposure is possible
Likely not all toxins have been ID

79
Q

How are mushroom poisonings treated?

A

Emesis
Activated charcoal after vomiting or gastric lavage
Catharic if no diarrhea