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VM 751 Toxicology > Tox Final > Flashcards

Tox Final Flashcards

1
Q

Most common snake bites are from what group of snakes and in what type of animal?

A 
pit vipers (crotalidae) - esp. copperheads
dogs
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2
Q

Coral snake

A
  • shy, non-aggressive, nocturnal
  • short, fixed, mem covered fangs w/ venom dripping out
  • delayed neurotoxic venom (little rxn at site) –> flaccid paralysis, resp paralysis
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3
Q

Coral snake bite treatment

A
  • Hospitalize at least 24 hrs b/c tox signs can take 12 + hrs to develop
  • supportive care, resp support, compression bandage, broad spec antibiotics
  • antivenin treatment discontinued
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4
Q

Pit vipers (rattlesnakes and cottonmouth)

A
  • retractable fangs + muscle cxn forces venom out
  • defensive (dry) or agonal bite (whole load)
  • venom meant to pre-digest, not kill
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5
Q

toxicity of rattle snake venom

A

rattle snake > water moccasin > copperhead

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6
Q

clin signs of diamondback bite

A

marked tissue destruction
coagulopathy
hypotension

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7
Q

clin signs of mojave A rattlesnake

A

minimal tissue destruction
no coagulation
severe neurotoxicosis

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8
Q

general clin signs of a pit viper bite (can be delayed)

A

regional swelling for ~36 hrs
ecchymosis & petechiation
+/- visible puncture wounds
tachycardia, shallow breathing, nausea, salivation, muscle twitch

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9
Q

treat a pit viper bite

A

baseline blood, recheck q6hrs to see level of evenomation
supportive care
Crofab antivenin - affects length of recovery, not survival chance

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10
Q

prognosis of pit viper bites

A

SA - good if early treatment

LA - survive initial bite, but often risk of dying w/ secondary tissue damage/infection

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11
Q

2 venomous lizards in US

A

Gila Monster

Mexican bearded lizard

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12
Q

venomous lizard bites

A
  • defensive only, don’t inject venom must be chewed in
  • longer bite duration = more evenomation
  • pain at bite site, tooth lacerations, regional muscle fasiculations but tissue necrosis rare
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13
Q

treat a venomous lizard bite

A

supportive care
broad spec antibiotics
narcotics or fentanyl for pain managment
prognosis good

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14
Q

Black widow bites

A
  • venom very potent (alpha-latrotoxin)
  • causes lactrodectism (muscle tightness/pain first few hours –> weakness/fatigue, insomnia)
  • cats very sensitive, get atonic paralysis & severe pain
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15
Q

treat a black widow bite

A

Lycovac antivenin

supportive - opiods, dizaepam (muscle rigidity)

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16
Q

(brown) recluse spider bite

A
  • bullseye lesion, slow to heal (6 mo - 1 yr)
  • venom has necrotizing enzymes, sphingomyleinase D
  • systemic signs rare
  • chemically debride lesion, drugs for pain, pruritis, infection, dapsone to inhibit neut migration
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17
Q

Are tarantulas dangerous?

A

US types - no

South America, Africa, Aus types - yes b/c neurotoxin (sometimes kept as illegal pets)

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18
Q

Scorpion sting (AZ bark scorpion)

A
  • venom has multiple toxins
  • sharp instant pain at site, edema, pruritis
  • maybe allergic rxn, systemic rxn
  • supportive care
  • debated if evenomation concerning in dogs/cats or not
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19
Q

Tick paralysis

A
  • 1 tick to infestation can cause
  • MOA of toxin unknown
  • ataxia –> paresis, flaccid paralysis –> resp failure, death
  • remove tick!! supportive care, topical insecticides
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20
Q

Bee stings

A
  • bronchiole constriction in cats
  • anaphylactic shock, secondary IMHA in dogs
  • remove stinger, supportive care, monitor for anaphylaxis
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21
Q

Botulism

A
  • limber neck (Bird), shaker foal synd (EQ)
  • ## Clostridum botulinum, multiple toxin types
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22
Q

Botulism MOA

A

toxin is protein, internalized by cell –> block ACh release –> progressive flaccid paralysis

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23
Q

3 ways to get botulism toxicity

A
  1. ingest preformed toxin (common in soil)
  2. Ingest spores (foals)
  3. wound contamination (e.g. castration)
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24
Q

Treat/prevent botulism

A

remove insiting cause (feed, debride) antitoxin, penicillin
prognosis guarded if have clin signs
prevent - toxoid vacc, good management

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25
Q

Tetanus MOA

A
  • Clostridium tetani w/ tetanospamin neurotoxin in soil
  • endocytosed into cells, block inhibitory NT release –> uncontrolled muscle contraction –> tetanty, sardonic grin, lock jaw, light sensitivity
  • EQ, rum more susceptible than dogs, cats
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26
Q

treat/prevent tetanus

A
  • penicillin, antitoxin tx, clean/debride wound
  • quiet dark space, maybe tranquilize
  • prognosis guarded w/ clin signgs
  • prevention key - good husbandry/mgmt, tetanus vacc
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27
Q

Cyanobacteria (blue-green algae)

A
  • risk factors: warm weather, increased nutrients (runoff) in water, algal blooms in late summer/early fall
  • increased wind concentrating cyanobacteria
  • often just see acute death
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28
Q

Microcystin or nodularin cyanobacteria toxicosis

A

hepatotoxic lethargic, vomiting, pale mucous mems, death in 24+ hrs

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29
Q

Anatoxin-a cyanobacteria toxicosis

A

muscle tremors, rigidity, resp distress/paralysis, convulsions, death in 30 min

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30
Q

Anatoxin-a(s) cyanobacteria toxicosis

A

SLUDGE, tremors, dyspnea, convulsions, death in 1 hr (resp arrest)

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31
Q

Treat cyanobacteria ingeston

A

Prevention is key - don’t eat
prognosis poor if have clinical signs, supportive care & decontaminate
atropine if anatoxin-a(s) - to blocK ACH while AChE blocked

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32
Q

Blister Beetles (aka Cantharidiasis)

A
  • beetles crushed in alfalfa, horse eats, cantharidin toxin (vesicant) rapidly absorbed in GI and conc in urine
  • acute colic, discomfort, bloody urine
  • enhance elimination, control pain, fix dehydration/electrolytes
  • prognosis poor, better if diagnosed early. Prevention!
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33
Q

Toad toxicity (FL, TX, AZ, CO, HI)

A
  • dogs
  • parotid glands on toad release toxin, absorbed in buccal mucosa
  • toxin is cardiac glycoside –> inhibit Na/K/ATPase pumps –> decreased AP’s
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34
Q

clin signs & treatment of toad toxicity

A
  • hypersalivation, vomiting –> convulsions, neuro –> coma, death w/in 15 mins sometimes
  • decontaminate - rinse mouth, supportive care
  • prognosis good if early decontaminate, don’t lick toads
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35
Q

Aflatoxins (from Aspergillus)

A
  • found in corn, usually exposure by feed contamination
  • metabolized into a reactive metabolite - carcinogenic, teratogenic, immunosuppressive
  • chronic exposure = liver dz
  • acute dose = emesis, diarrhea, convulsions, epistaxis, death
  • prevention key, activated charcoal + oxytetracycline for hepatic damage - recovery prolonged/incomplete
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36
Q

Citrinin & Ochratoxin (aspergillus, penicllium spp)

A
  • grains, beans, black pepper, coffee, etc.
  • pigs and rats
  • Porcine mycotoxin nephropathy
  • enterohepatic recycling = longer half life, accums in kidneys
  • chronic = kidney dz
  • acute = gastroenteritis, emesis, tenesmus, etc
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37
Q

Why are ruminants relatively immune to ochratoxin toxicosis?

A

rumen microbes cleave the toxin into an non-toxic form

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38
Q

Ergot (Claviceps spp)

A
  • grasses, cereal grains
  • 5-HT(serotonin) agonist, Dopamine antagonist, NE agonist
  • cause vasoconstriction
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39
Q

4 forms of Ergot toxicosis in livestock

A
  1. Cutaneous & gangrenous lesions (tail, extremities)
  2. Hyperthermia, production loss
  3. Repro failure (weak foals, stillborns)
  4. convulsive/neuro form (acute ingestion of large dose)
    fescu foot
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40
Q

Trichothecenes (Fusarium spp)

A
  • contaminated feeds during flowering, seed development (high rain, humidity) + delayed harvest
  • most animals recover rapidly except pigs (highly sensitive, can’t metabolize vomitoxin –> vomiting)
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41
Q

Zearalenone (Fusarium spp)

A
  • corn, stable in environ
  • pigs, mebe sheep
  • enz’s that produce acid are induced at low temps –> clin signs freq in colder areas
  • enterohepatic recycling = increased half life
  • acts as weak estrogen: swelling/redness of female parts, ovarian atrophy, weight gain
  • remove contamination, PG F2- alpha can correct anestrus
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42
Q

Fumonisin

A
  • ELEM (eq encephalomalacia) or PPE (porcine pulmonary edema)
  • cattle resistant
  • guidelines for max allowed in feed
  • no treatment
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43
Q

ELEM clin signs

A

MOA not understood - cardio dysfunc

Neurotoxic and hepatic syndrome

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44
Q

PPE clin signs

A

MOA - inhibit myocardial Ca channels –> decreased contractility
3-6 days post exposure
L sided heart failure, pulmonary edema –> dyspnea/tachypnea, cyanosis, sudden death

45
Q

Tremorgenic Mycotoxins - “Staggers”

A

reduce GABA, glutamate –> prolonged depolarization –> neuro probs, ataxia etc.
vasoconstriction in cerebrum can –> cerebral anoxia
clin signs in ~7 days but resolve in few days once exposure removed

46
Q

Slaframine - “Slobber syndrome” or “clover poisoning)

A
  • Rhizoctonia leguminicola fungus synthesized indolizidine alkaloid from lysine = black patch on clover
  • active form (ketoimine metabolite) is parasympathomimetic agent –> stim’s salivation in ~15 mins
  • atropine can stop activity, but not reverse effects
  • remove contaminant
47
Q

Fescue grass + N. coenophialum (fungal endophyte)

A

Produces ergot alkaloids

Fescue foot, summer syndrome, fat necrosis or lipomatosis

48
Q

Penitrem A & Roqefortine

A

blue moldy cheese

crosses BBB –> CNS issues in Dogs (tremors –> death)

49
Q

How does radiation affect the body

A
  • damages genetic structure, then cells die during division (mitotic death)
  • can kill organ or animal itself
50
Q

ARS (acute radiation syndromes)

A 
Occur w/ whole body radiation
Cerebrovascular syndrome
GI syndrome
Hematopoietic syndrome
Pulmonary syndrome
Cutaneous radiation injury syndrome
51
Q

Cerebrovascular syndrome

A

acute, >50 Gy dose
radiation neurotoxin –> disrupt BBB, circ –> perivascular edema and hemorrhage
nausea/vomiting, disoriented, discoordinated, resp distress, seizure –> death in 72 hrs

52
Q

GI syndrome

A

7+ Gy dose

nausea, vomiting, diarrhea –> septicemia, shock –> death in 3-10 days

53
Q

Hematopoietic syndrome

A

3-8 Gy dose
severity depends on individual, level of exposure
bone marrow stem cell destruction –> pancytopenia
clin signs occur after pancytopenia
chills, fever, bruising, etc. - impaired immune sys, impaired coag –> death before anemia develops, 1-2 mo post exposure
<5 Gy exposure, supportive care; 8-10 Gy = small window for bone marrow transplant

54
Q

pulmonary syndrome (rare)

A

> 8 Gy

animals that survived hematopoietic syndrome still could die in ~30 days b/c of inflammatory pneumonitis

55
Q

Cutaneous radiation injury syndrome

A

ARS’s usually have some level of skin damage
inflammation, erythema, dequamation, etc.
may have latent phase
Can be independently lethal or complicate recovery from hematopoietic

56
Q

Prodromal radiation syndrome

A

radiation sickness that can preceed any ARS, may predict outcome
latent
easily fatigued, anorexia, vomiting
patient recovers or dies

57
Q

low dose irradation vs. high dose whole body irradiation

A

low dose: late effects like genetic change, cancer

high dose: acute effects, likely death

58
Q

What is the main concern about radiation exposure?

A

smaller doses over a longer period of time –> cancer

biological effects depend on absorbed dose (stochastic - random)

59
Q

RBE (radiation biological effectiveness)

A

helps determine how efficient a type of radiation is at producing biological effect
approximated using WR (Radiation weighting factor)

60
Q

Radiation Protection Equivalent Dose

A 
combines physics (absorbed dose) with RBE (biology) to estimate injury
ED (equivalent dose) = absorbed dose x WR
Equivalen dose x Wt = effective dose
61
Q

the annual radiation occupational limit for a radiation worker

A 
5 Rem (= 50 mSv)
aka the stochastic random risk of getting cancer
Lifetime dose shouldn't exceed yrs age x 1 REM
62
Q

Who watches over radiation safety?

A

OSHA - checks for failures of compliance
ICRP/NCRP (US version) - makes reports that determine policy
EPA, nuclear regulatory council, DOE, OSH, states implement policy

63
Q

what must the principal user or vet radiation safety office do

A

provide instruction to personnel on safety
provide documentation
responsibilities extend to vets who aren’t primary user b/c operating x-ray equipment = small but definite radiation risk

64
Q

What happens to pregnant employees?

A

give voluntary written notice to principal user

additional monitoring, keep exposure below 0.05 rem/mo

65
Q

ALARA (as low as reasonably achievable)

A

common sense + education
provide rules and documents, dosimeters, follow the rules
Time, distance, shielding

66
Q

Mercury toxicity

A
  • metallic mercury is a liquid - vapors are the problem
  • water converts methy murcury –> di-methly mercury which is lipid soluble
  • targets nervous, renal, cardio, GI, hematopoietic
67
Q

diagnose mercury toxicity

A

History most important
Acute - hg levels in blood, urine, liver, kidney
Chronic - test hair
Can only treat acute - egg white, charcoal, then succimer

68
Q

Mercury PM

A

Gastric ulcers
tubular necrosis
cerebellar hypoplasia w/ MeHgs

69
Q

Arsenic toxicity

A
  • don’t burn treated wood
  • As binds to lipoic acid affects TCA cycle, energy metabolism
  • targets actively dividing cells (high oxidative E use), intestinal epithelium, epidermis, kidney, liver
  • clin signs: abdominal pain, ataxia, watery diarrhea, dehydration
70
Q

Diagnose As toxicity

A

Urine or liver As levels above diagnostic levels

Hair if chronic exposure

71
Q

Treat As toxicity

A

Detox - Dimercaprol (pulls arsenic off lipoic acid), Succimer

72
Q

Arsenic PM

A

GI tract erythema, petechia & accumulation of fluid

epithelial necrosis

73
Q

Lead (Pb) toxicity

A
  • most common heavy metal toxicity
  • in muscle not toxic (walled off), ingested = toxic b/c in acidic environment
  • target tissues: CNS (primarily), hemolymphatic system, GI
74
Q

Sources of Pb

A

batteries - most common in cattle
lead based paints
shot, weights, smelter exposure, etc.

75
Q

Pb toxicity MOA

A
  • absorbed in GI by active transport using Ca absorption mech (where Ca is, lead will be)
  • Binds to RBC’s, accums in soft tissue, bone (chronic)
76
Q

Diagnose Pb toxicity

A

whole blood sample

77
Q

Pb toxicity clin signs

A

Very common to not see anything clinically
Blindness, headpressing in run
roaring in EQ, anemia in cats
aggression, anorexia

78
Q

Diagnose Pb toxicity

A

Hx of clin signs
Immature RBC’s w/ basophilic stippling
whole blood Pb levels above diagnostic levels (or kidney, urine)
Radiographs - Pb objects in GI

79
Q

What 3 Metal/Feed toxicities are hard to differentiate between?

A

Lead poisoning
PEM
Water deprivation

80
Q

Treat lead poisoning

A

Ca-EDTA, Succimer

Remove lead from GI if seen

81
Q

Pb toxicity on PM

A

Rumen - laminar cortical necrosis, lead pieces
Rental tubular epithelium degeneration, necrosis
Intranuclear inclusion bodies
Waterfowl - muscle wasting, Pb shot in gizzard

82
Q

Molybdenum (Mo) Toxicity & Copper deficiency causes

A

Primary Cu deficiency - low Cu in diet
Secondary Cu deficiency - High Mo in diet –> low Cu
High Sulfur intake - potentiates Mo, often from water

83
Q

Molybdenum (Mo) Toxicity & Copper deficiency

A

Low Cu = low Cu enzymes
First see low Cu in liver where it’s absorbed, serum Cu will remain normal
After serum levels decrease, see low Cu enz & clinical signs affecting all tissues

84
Q

Molybdenum (Mo) Toxicity & Copper deficiency clinical signs

A

Chronic diarrhea (when Mo high)
Bleached dull hair, spontaneous fractures, decreased production & immune response
ADR (ain’t doing right)
Swayback in lambs, kits

85
Q

Swayback

A

lambs, kits only NOT rum

sheep fetus doesn’t accumulate Cu in liver during gestation but cattle fetus does

86
Q

What can decrease copper utilization

A

Dietary Mo and sulfur

Excess zinc, iron

87
Q

Diagnose Molybdenum (Mo) Toxicity & Copper deficiency

A

Serum Cu low, serum Mo high
liver Cu levels low
Determine dietary Cu and Mo (Should be <4 Cu : 1 Mo)
Determine dietary S & Mo (should be <100 S : 1 Mo)
PM - no diagnostic signs

88
Q

Treat Molybdenum (Mo) Toxicity & Copper deficiency

A

Increase dietary Cu: Mo ratio w/ special salt/trace mineral mix
CuO boluses given PO
careful w/ sheep - susceptible to Cu toxicity

89
Q

Cu toxicity

A

Mostly a sheep, goat problem

  • Don’t feed EQ, Pig, Poultry feeds to sheep or cattle (higher in Cu)
  • Don’t let sheep graze in pasutres w/ pig or poultry manue
  • Accidental oversupplementation –> accum in liver, then affects blood, renal causing damage
90
Q

Clin signs of Cu toxicity

A

~2 weeks before signs, already liver is necrosing but liver values may not be particularly high until hemolytic crisis already occuring
serum Cu may/not be changed depending on chronicity
Hemoglobinuria, Icterus, anoxia, death

91
Q

Treat Cu toxicity

A

Focus on reducing risk in rest of herd

Feed a Cu deficient diet, add thiomolybdate

92
Q

PM signs of Cu toxicity

A

Gunmetal blue kidney

liver is swollen, friable w/ fibrosis in portal areas, bile duplication

93
Q

Zinc toxicity (Zn)

A
  • dogs, sometimes birds
  • pennies minted after 1982, galvanized surfaces, industrial
  • MOA some kind of enz inhibition –> RBC membrane damage, oxidative damage
    Target tissue: GI, RBC’s
94
Q

Zn toxicity clin signs

A

Dog, cat - vomiting, diarrhea, icterus, Hemogobinuria & emia, anemia

Birds - depress, anorexic, wt loss, fluffed feathers, seizure

95
Q

Diagnose Zn toxicity

A

Radiographs
Royal blue tops for serum Zn (no hemolysis)
Regenerative hemolytic anemia w/ basophilic stippling, heinz bodies, nucleated RBC’s
PM - non-specific gross pathology - hepatic hemosiderosis & hepatocellular necrosis

96
Q

Treat Zn toxicity

A

remove foreign object from GI
supportive care, blood transfusion
Ca-EDTA for birds

97
Q

Sulfur toxicity

A
  • Large animals
  • High SO4 in water, or plants in high S soils, molasses-based diets, corn gluten
  • Sulfur reduced by rumen bacteria –> sulfide –> sulfide absorbed in blood or lungs –> inhibits cytochrome sys –> decreased energy production
  • target: CNS
98
Q

Clin signs of sulfur toxicity

A

blindness, head pressing, recumbency, anorexia

99
Q

Diagnose sulfur toxicity

A

Determine water and feed So4 levels (total dietary level)

Hard to differentiate between Pb and water deprivation

100
Q

Treat sulfur toxicity

A

supportive care
decrease S intake, feed roughage
Thiamine if treating for PEM

101
Q

PM findings from sulfur toxicity

A

Rotten egg smell from rumen, rumen contents black

PEM in brain (polioencephalomalacia) - necrosis, softening, swelling

102
Q

Water deprivation/salt toxicity

A
  • brine water, or high dietary salt + limited water intake, restricted water intake (4-7 days to develop)
  • Increased serum Na –> increased brain, CSF Na –> increased glycolysis & energy –> excess Na trapped in brain, CNS
  • clin signs: blindness, wandering, head pressing, depression, weak
103
Q

Diagnose Water deprivation/salt toxicity

A

History, dehydration status
serum, CSF Na values
Hard to differentiate between PEM & Pb toxicity
PM - cerebral edema, test aqueous or vitreous humor for Na levels

104
Q

Treat Water deprivation/salt toxicity

A

rehydrate slowly over 48 - 72 hours otherwise cause more probs
IV hypertonic saline to reduce cerebral edema

105
Q

Urea/Non protein nitrogen toxicity

A
  • additive in feedlots
  • increased blood, brain NH3 –> decreased ATP, citric acid, etc. increased lactate
  • muscle tremors, weakness, colic
106
Q

Diagnose Urea/Non protein nitrogen toxicity

A

Hx, Rumen pH >8.0
Dietary urea analysis
Rumen fluid, vitreous fluid, serum NH3
PM - no lesions, rumen pH >8.0

107
Q

Treat Urea/Non protein nitrogen toxicity

A

Infuse rumen w/ 5% acetic acid (vinegar) or cold water

Preventions - limit NPN to <3%, don’t feed NPN w/ full roughage diet

108
Q

Ionophores

A
  • promote growth in cattle
  • alters rumen fermentation –> increased propionate, acidosis
  • concentrates in liver - can cause toxicity/damage at high conc’s
  • anorexia, sweating, colic, hypotension, death
109
Q

Use succimer to treat what?

A

arsenic
mercury
lead toxicities

VM 751 Toxicology (2 decks)

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