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Veterinary Toxicology > Hematotoxicology > Flashcards

Hematotoxicology Flashcards

1
Q

What is the difference between primary and secondary hematotoxicosis? What are the main 4 clinical manifestations?

A
  • PRIMARY = direct effect of toxin/toxicant on blood elements
  • SECONDARY = impairment of other tissues (liver, kidney) or systemic disturbances that affect blood elements

methemoglobinemia, hemolysis, coagulation defects, anemia

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2
Q

Where are vipers found in the US? When are bites most common? What causes 99% of these bites?

A

all states except HI, ME, and AK - (pygmy) rattlesnakes, Massasauga water moccasins, cottonmouths, copperheads

April - October

pit vipers

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3
Q

What 5 anatomical structures do pit vipers have?

A
  1. triangular head
  2. elliptical pupil
  3. heat sensing pit
  4. retractable fangs
  5. rattle-like tail
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4
Q

What is the main component of snake venom? What are the 2 components of the toxic principles?

A

90% water, > 50 enzymatic and non-enzymatic components

  1. ENZYMATIC: collagenase, hyaluronidase, protease, phospholipase, phosphodiesterase
  2. NON-ENZYMATIC: coagulants/anticoagulants, myotoxins, neurotoxins, cardiotoxins, lipids, acids, cations, nucleotides
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5
Q

What 5 victim variables affect the severity of envenomation?

A
  1. species and body mass
  2. bite location and post-bite behavior
  3. time to medical attention
  4. type of first aid applied
  5. concurrent medications (NSAIDs)
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6
Q

What 5 snake variables affect the severity of envenomation?

A
  1. species
  2. age/size - young snakes most dangerous
  3. motivation for bite - defense, offense, agonal
  4. time since last venom use - takes 21 days to replenish
  5. time of the year
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7
Q

What 3 characteristics affect victim response to venom?

A
  1. species of snake
  2. volume of venom injected
  3. species of bite recipient
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8
Q

What are the 3 possible presentations of rattlesnake envenomation?

A
  1. tissue destruction, coagulopathy, hypotension (classic syndrome - diamondbacks)
  2. neurotoxicosis (Mojave)
  3. combination
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9
Q

What is the primary purpose of venom? What are the 4 main mechanisms based on the fractions of the venom?

A

immobilize prey and predigest its tissues

  1. enzymatic/spreading factors - breakdown connective tissue to allow for rapid penetration and spread of toxins (hyaluronidase, collagenase, protease, phospholipase)
  2. myotoxins - destroy muscle tissues by opening NA+ channels causing hypercontraction and rupture of myofibrils
  3. coagulants - hyper/hypercoagulation, dissolution of clots
  4. cardiotoxins - depress heart function
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10
Q

What do the cardiovascular toxins, neurotoxins, and nonenzymatic toxins of rattlesnake venom do?

A

induce local pain, tissue necrosis, and hypotension

inhibit release of neurotransmitters

(killing factors) - potentiate venom by up to 50x

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11
Q

Are all rattlesnake bites venomous? How do clinical signs compare in cats and dogs?

A

not necessarily - 25% of bites are dry

cats are more resistant, but are brought into the vet in worse states

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12
Q

What clinical signs are commonly observed with rattlesnake envenomation? What results from the increased vascular permeability?

A
  • fang wounds
  • pain, severe hypotension
  • coagulopathies, ecchymosis, petechiation
  • discoloration of the skin
  • tachycardia, shallow respiration, shock
  • weakness, nausea
  • muscle fasciculations, salivation, enlarged regional lymph nodes

regional swelling, pale or congested mucous membranes

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13
Q

Rattlesnake envenomation, clinical signs:

A
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14
Q

How can rattlesnake envenomation be diagnosed on a blood smear?

A

non-EDTA blood smear - echinocytosis (burr cells)

  • coagulation profile (ACT, PT, aPTT)
  • no definitive confirmatory test
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15
Q

What 3 first air measures should be done following a viper bite?

A
  1. keep patient calm - physical activity and anxiousness can promote rapid uptake of venom
  2. keep bite site below heart level
  3. transport patient to veterinary facility
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16
Q

What 6 first aid measures should be avoided following a viper bite?

A
  1. ice, cold/hot packs, sprays
  2. incision and suction
  3. tourniquets
  4. administration of aspirin or tranquilizers
  5. waiting for envenomation before seeking care
  6. electroshock

(no first aid measure for pit viper bite victims prevents morbidity/mortality)

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17
Q

What 2 things should be monitored in patients bit by pit vipers? What 4 medications can be given? What is avoided?

A

hemostasis/biochemistry panels and diameter of swelling

  1. early IV antivenom
  2. aggressive IV crystalloid fluid therapy
  3. antibiotics
  4. antihistamines - calming, does not prevent allergic reactions

corticosteroids - risks clotting anomalies

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18
Q

What is recommended when antivenoms are not administered following a pit viper bite? What is avoided?

A

IV narcotics to control pain - Fentanyl

Morphine —> causes histamine release

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19
Q

What are the 2 generations of anticoagulant rodenticides? How does the second generation compare to the first?

A
  • FIRST GEN = warfarin, chlorophacinone, diphacinone, pindone
  • SECOND GEN = bromadialone, brodifacoum, difenacoum, difethialone

have enhanced toxicity

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20
Q

Secondary poisoning caused by anticoagulant rodenticides is uncommon. In what 2 species does this tend to occur? What animals are most sensitive?

A
  1. barn cats
  2. birds of prey

dogs > cats + 2nd gen are more toxic

21
Q

Where are anticoagulant rodenticides absorbed? How does it tend to travel in the body? What makes NSAIDs increase their toxicity?

A

well-absorbed from GIT (slow absorption for warfarin)

highly plasma protein bound with a low Vd —> NSAIDs displace the rodenticides from the plasma proteins

22
Q

Where are anticoagulant rodenticides metabolized? Excreted? What can be used to lower toxicity?

A

liver —> mixed function oxidase (MFO)

kidney

MFO inducers - Phenobarbital

23
Q

How do ruminants and swine compare in their sensitivity to anticoagulant rodenticides?

A

cats and dogs most susceptible

  • ruminants are less susceptible than monogastrics
  • swine are sensitive to warfarin
24
Q

What is the mechanism of toxicity of anticoagulant rodenticides? What 4 risk factors increase toxicity?

A

block the synthesis of vitamin K-dependent clotting factors (II, VII, IX, X) by competitively inhibiting vitamin K epoxide reductase and halting the recycling of vitamin K by the liver

  1. age
  2. high fat diet
  3. oral antibiotics
  4. hepatic disease
25
Q

When do clinical signs of anticoagulant rodenticide poisoning start? What are common signs?

A

preformed factors are not affected, so clinical signs appear when these factors are depleted, typically within 3-5 days

  • blue-green feces
  • lethargy, exercise intolerance
  • anorexia, weakness
  • dyspnea due to bleeding in chest cavity
  • lameness and bruising
  • hemorrhaging through nares/rectum, brain/spinal cord (neurologic disease), placenta (abortion)
26
Q

What should be assumed if the particular rodenticide consumed is unknown? How is toxicosis diagnosed?

A

assume it is long-acting

  • clinical signs and pathology
  • CBC, serum chemistry
  • radiography
  • thoracentesis and abdominal paracentesis
  • coagulation tests (OSPT, aPTT, ACT prolonged)
  • chemical analysis of liver, blood, and bait
27
Q

What effect do anticoagulant rodenticides have on the different pathways of the coagulation cascade? What coagulation test is the most sensitive?

A
  • EXTRINSIC: effects seen within 10-12 seconds (FVII has the shortest half-life)
  • INTRINSIC: effects seen within 5-15 mins

OSPT - measures EXTRINSIC pathway
(ACT measures the INTRINSIC pathway and is less sensitive, since it requires IX, X, and II to be <5% of normal)

28
Q

What are 4 common treatments for anticoagulant rodenticide poisoning?

A
  1. decontamination for recent exposure (emesis + activated charcoal)
  2. blood/plasma transfusion
  3. vitamin K
  4. supportive care: oxygen, exercise restriction, antibiotics, IV fluids, pleural tap
29
Q

What differential diagnoses should be ruled out of anticoagulant rodenticide poisoning?

A

other causes of hemorrhage

  • DIC
  • hemophilia
  • von Willebrand’s disease, especially in Scottish terriers, Dobermans, and Welsh corgis
  • liver disease
  • canine ehrlichiosis
30
Q

What is the toxic principle in Melilotus spp. (white and yelllow sweet clover)? Where has toxicity been reported?

A

dicoumarol - dicoumarin or dihydroxycourmarin

OH, IN, IL, WI, SD, ND, NE

31
Q

What species are most commonly poisoned by sweet clover? When does poisoning most commonly occur?

A

cattle —> more likely to accept damaged/sweet clover hay
(horses, pigs, and sheep can also be poisoned)

winter, when animals are fed moldy sweet clover hay or silage (hay made in wet summers is a risk factor)

32
Q

How does sweet clover become toxic? What conditions favor this? What is its metabolism like?

A

soil fungi (Aspergillus, Arthrobacter, Penicillium, Hemicolor, Fusarium, and Mucor) on stems of sweet clover convert naturally coumarin glycoside into dicoumarol

cutting and bailing clover under high moisture

readily absorbed in the GIT, metabolized in the liver by MFO, and excreted through urine

33
Q

What is the mechanism of toxicity of sweet clover?

A

competitively inhibits vitamin K epoxide reductase essential for regenerating the active form of vitamin K, reducing vitamin K-dependent coagulation factors (II, VII, IX, X) —> hemorrhaging

34
Q

What are some common clinical signs of sweet clover poisoning?

A
  • hemorrhaging from natural orifices and into muscle, eyes, brain, lungs, and heart
  • prolonged hemorrhaging from surgical sites (after castration and dehorning)
  • anemia
  • large subcutaneous hematomas that are painless and not hot to the touch (in mesentery = colic)
  • swollen joints (lameness), recumbency, death
  • tachycardia, tachypnea
  • abortion
35
Q

How do cattle become intoxicated by sweet clover? How is it diagnosed?

A

exposure to sweet clover hay/silage, not grazing from the pasture —> will not be moldy

  • elevated clotting times
  • herd is affected, not individual (ruling out blackleg, pasteurellosis, bracken fern poisoning, and aplastic anemia)
  • analyze hay/silage for dicoumarol
36
Q

How is sweet clover poisoning treated?

A
  • remove suspect hay/silage and replace with alfalfa or good quality grass
  • correct hypovolemia and clotting factor deficit with blood transfusions
  • administer vitamin K
  • supportive care: quality feed, ample freshwater, avoid stress
37
Q

What is the most common source of nitrates? When do they accumulate in plants? In what 2 conditions are they particularly high?

A

plants, water runoff, fertilizers, sodium nitrite food preservatives

when plants are grown under stressful conditions (herbicides, drought, hail/frost)

  1. just before flowering
  2. drying (hays)
38
Q

Nitrate accumulating plants:

A
39
Q

Where is most of the nitrate found in plants?

A

97% in the stem

40
Q

What animals are most susceptible to nitrate toxicosis? Why? What animal is less susceptible?

A

cattle - contain nitrate-reducing microbes in their rumen
(in horses, nitrate reduction happens lower in the GIT and liver)

sheep - lower rate of plant intake and shorter elimination

41
Q

What 4 factors contribute to nitrate toxicosis susceptibility?

A
  1. rate of intake
  2. GI nitrate reduction
  3. diet
  4. metabolic state of the animals
42
Q

How is nitrate metabolized in ruminants?

A
  • upon ingestion, nitrate is reduced into nitrite by rumen microbes
  • nitrate and nitrite anions are readily absorbed from the GIT (nitrite can also cross placenta)
  • nitrate is eliminated in the urine, with ruminants eliminating a lower proportion
43
Q

What is the mechanism of toxicity of nitrate?

A

after nitrate is reduced into nitrite, it is able to oxidize the Fe2+ in hemoglobin into Fe3+ (metHb), which has a decreased oxygen carrying capacity and deprived tissue from oxygen

  • 30-40% metHb induces mild clinical signs
  • > 80% metHb is lethal
44
Q

How else does nitrate poisoning alter oxygen delivery to tissues other than forming methemoglobin?

A

nitrite is able to cause vasodilation and reduces vascular tone

45
Q

ADME and MOT of nitrate:

A
46
Q

What do the acute clinical signs of nitrate toxicosis reflect? What are some common signs? What can exacerbate these signs, making them fatal?

A

tissue oxygen deprivation

  • exercise intolerance, weakness, dyspnea
  • tachycardia, tremors
  • depression, collapse
  • cyanotic MM
  • ataxia, recumbency, terminal convulsions
  • diarrhea, vomiting, and salivation due to GIT irritation (fertilizers)

forced movement or restraint

47
Q

What are the common chronic clinical signs of nitrate toxicosis? What is especially seen in sheep?

A
  • abortion (“lowland abortion syndrome”)
  • poor growth and feed efficiency
  • decreased milk production
  • infertility
  • increased susceptibility to infection

goiter - nitrate interferes with iodine metabolism

48
Q

What is the antidote for nitrate toxicosis? How else can it be treated?

A

IV methylene blue with dose depending on severity of toxicosis

  • avoid stress
  • rumen lavage
  • oral penicillin

Veterinary Toxicology (29 decks)

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