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Toxicology > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What factors in plants increases risk of mycotoxin production?

A

Stress due to drought, flooding, poor soil fertility

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2
Q

How are mycotoxins distributed in feed?

A

Unevenly, in pockets. Toxins can persist after fungi are gone.

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3
Q

What animals are most susceptible to mycotoxins?

A

Monogastrics are at highest risk (poultry, swine), Horses are monogastrics, but at less risk, ruminants least susceptible, but pre-ruminants are fully susceptible

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4
Q

What is the potential role of mycotoxin contamination in causing animal health problems?

A

If animals eat contaminated feed can cause drop in production directly or due to secondary infection.

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5
Q

What are the risk factors associated with the formation of mycotoxins in feed ingredients? Does mold mean that there is mycotoxin present?

A

Stress to plants, less likely in surface “spoilage” organisms, more likely to produce mycotoxins if infecting living tissues, highly dependent on environmental factors and mold ≠ mycotoxins.

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6
Q

What are some feeding situations that could be associated with ingestion of mycotoxins?

A

Monogastric animals eating corn or cereal grains. Whole oil seeds. Cattle eating mycotoxin-positive feed in large amounts.

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7
Q

What are some clinical signs that could be associated with ingestion of mycotoxins? What other diseases are rule outs?

A

Key sign of mycotoxicosis is feed refusal. Also ill-thrift, weight loss, usually all animals in group. Can be immune suppressive, leading to secondary infections. Rule outs are subclinical metabolic, nutritional, or infectious diseases.

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8
Q

How would you test for mycotoxins?

A

Start by testing whole diet, then feed ingredients. Black light for Aspergillus, on site qualitative tests, full wet chemistry testing

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9
Q

How would you treat and prevent mycotoxin contamination?

A

Once mycotoxin concentrations known, remove or dilute feed and wait >1 week to observe for improvement. Could try binders. Best approach is to prevent fungal growth in the first place. Prevent storage contamination- harvest, store, silage properly. Use preservatives. Delay grinding, avoid screenings.

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10
Q

Name some common mycotoxins and where they are found/sources.

A

Aflatoxin (warm climates, high humidity) corn, potatoes, wheat, soy, peanuts, distilled products
Fumonisins (corn especially broken/screenings)
Zearalenone (corn, other grains) ‘pink ear rot’ ‘scab’
Trichothecens (corn)
Ergot (Ryegrass)
Slaframine (clover, clover hay) ‘slobbering factor’
Tremorgens (Grasses, spoiled foods/garbage)

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11
Q

What are the primary effects of aflatoxin? Most susceptible species?

A

Hepatotoxocitiy, carcinogenesis. Swine most sus. Regulated in milk bc carcinogenic in humans. Young animals more sensitive. Stunted growth. Acute- hemorrhage, bloody diarrhea death. Chronic- icterus, fatty liver, anemia, ascites.

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12
Q

What are the primary effects of fumonisins? Most susceptible species?

A

Leukoencephalomalacia in horses most sensitive (CNS, death), also swine (porcine pulmonary edema due to heart failure in pigs)

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13
Q

What are the primary effects of Zearalenone? Most susceptible species?

A

Weak Estrogen. Swine most affected. Vulvar issues, infertility, prolapse.

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14
Q

What are the primary effects of Trichothecens? Most susceptible species?

A

T2 toxin- immunosuppression in pigs. DON/Vomitoxin! Swine most sus, also small ruminants (vomiting! Rare)

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15
Q

What are the primary effects of Ergot? Most susceptible species?

A

Extreme vasoconstriction, gangrene/sloughing of extremities. Cattle.

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16
Q

What are the primary effects of Slaframine? Most susceptible species?

A

Horses ‘slobbering factor’, excessive salivation key sign

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17
Q

What are the primary effects of Tremorgens? Most susceptible species?

A

CNS overstimulation and tremors. Grazing animals

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18
Q

What type of compound is Monensin? What is it used for?

A

Polyether Acid Ionophore Antibiotics. Not useful for pathogens, alters rumen biota favorably.

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19
Q

What is the method of action for Monensin?

A

Alters ion channels in cell walls, heart and skeletal muscle most affected.

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20
Q

What species is monensin approved for use in? Is it always safe in these species?

A

monensin is approved for cattle, goats, chickens, turkeys, and quail. Still toxic if overdosed.

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21
Q

What species are most susceptible to Monensin toxicity? Clinical signs?

A

Sensitivity varies with ability to oxidize monensin. Horses very sensitive, cows much less sensitive. Neuro signs, cardiac muscle in horses, skeletal muscle cattle. CHF key sign in horses.

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22
Q

How can you prevent monensin toxicity?

A

Feed mills cleaning equipment to avoid cross-contamination, avoid totally in small mixed species operations to prevent cross-contamination.

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23
Q

Would you feed cotton products to monogastrics? Why?

A

No. Gossypol. unbound toxic. Ruminants bind 8x more than monogastrics.

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24
Q

What is gossypol? Who is it toxic to?

A

Yellow pigment found in cotton plant at highly variable concentrations. Free Gossypol is toxic to all animals- less so to cattle bc bound in rumen. Cotton seed is main concern.

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25
Q

What are the effects/Clinical signs of Gossypol toxicity? Treatment?

A

Cardiotoxic- cardiac arrhythmia, Congestive heart failure. Yellow fluid. At low level, fertility issues. No specific treatment. Cotton products not usually fed to monogastrics.

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26
Q

What is urea/NPN and why is it fed to cattle?

A

Nitrogen sources. Rumen microbes make protein from ammonia and carbohydrates, so these are a cheap protein source, but can be toxic.

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27
Q

What are possible issues with feeding urea/NPN to cattle? How would you test for and treat for toxicity associated with them?

A

When rumen pH becomes high enough, NH4+ converts to NH3 which can diffuse out and overwhelm liver. Results in ammonia-induced encephalopathy, cyanosis, death. Test Ruminal pH, if pH >7.5, treat with cold acetic acid to re-acidify rumen and prevent NH4+ to NH3 and diffusion out of the rumen.

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28
Q

What is salt poisoning/water deprivation? What species does it affect?

A

Excessive salt in diet, sudden increase in salt, inadequate water. Affects all species, pigs most often due to drinking nipple issues. Sheep least susceptible.

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29
Q

What are the Clinical signs of salt poisoning? Treatment?

A

CNS signs due to hypernatremia, death from respiratory failure. Acute GI signs. Treat by gradually adding water.

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30
Q

What are the clinical signs of iodine toxicity in cattle?

A

Lacrimation, epidermal sloughing (dandruff)

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31
Q

How does tall fescue poisoning happen? What are sensitive species and clinical signs?

A

Type of ergot poisoning, once infected, propagated through seeds, most fescue in US infected. Cattle and horses- grazers. Key signs: ‘summer slump’ in grazing cattle, repro issues in brood mares.

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32
Q

What feed toxin has a specific treatment and what is it?

A

Urea/NPN. If ruminal pH > 7.5, treat with cold acetic acid.

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33
Q

What herbal supplements are toxic?

A

Chamomile, garlic, Echinacea, essential oils

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34
Q

List 5 predisposing factors for toxicity in the liver

A

First-pass effect
Enterohepatic circulation
Unique functions (bile formation/excretion)
Major metabolism site (bioactivation)
Zones affected differently due to blood/oxygen supply (lowest zone 3)

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35
Q

Describe 5 different ways toxicity can lead to liver injury

A

Hepatocytotoxicity, Fatty liver, Cholestasis, Bile duct dam, Cirrhosis, Vascular, Tumors

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36
Q

What are 4 different types of liver injury and what are the clinical measures of that function?

A

Hepatocyte injury: ALT↑, AST↑, bilirubin↑
Cholestasis: ALP↑, GGT↑, bilirubin↑, cholesterol↑
Liver mass decreased: urea↓, albumin↓, cholesterol↓, coagulation factors↓
Portal blood flow: ammonia↑, bile acids↑, globulins↑

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37
Q

What are sequelae of chronic liver failure?

A

GI signs, depression, icterus, reduced milk production, increased sensitivity to toxicity, photosensitization in grazing animals, hepatic encephalopathy

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38
Q

What are the clinical signs and diagnostic abnormalities of acetaminophen toxicity?

A

CS: BLOOD + LIVER Depression, Tachypnea, Cyanosis, facial edema, chocolate colored blood
Diagnostic Abnormalities: elevated ALT/bilirubin

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39
Q

What is the mechanism of action and specific treatments for acetaminophen?

A

MOA: Oxidizes Hb to MetHb in dogs and cats only. CYPs convert acetaminophen to NAPQI-> hepatotoxicity.
Specific treatments: Antioxidants (NAC/SAM), Cimetidine in dogs only to block formation of NAPQI, Methylene Blue

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40
Q

What are the clinical signs and diagnostic abnormalities in amanita mushroom toxicity?

A

CS: GI + LIVER Initial GI phase, latent 12-24 hrs, final phase of liver failure, death
Diagnostic Abnormalities: elevated ALT/bilirubin

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41
Q

What is the mechanism of action and specific treatments for amanita mushrooms?

A

MOA: Amatoxins bind RNA polymerase, high protein synthesizing cells most sensitive. Phallotoxins and
virotoxins irreversibly polymerize hepatic actin filaments, triggering hepatic cholestasis. VERY TOXIC. enterohepatic circulation.
Specific treatments: NAC/SAM!! Transfusion, Vitamin K.

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42
Q

What are the sources, clinical signs and diagnostic abnormalities for blue green algae toxicity?

A

Sources: stagnant water, ponds, drinking water.
CS: GI or LIVER or CNS BASED ON TYPE Vomiting, Hyporexia, weakness, photosensitization in LA
Diagnostic Abnormalities: elevated ALT/bilirubin

43
Q

What is the mechanism of action and specific treatments for blue green algae?

A

MOA: Microcystin inhibits phosphatases in hepatocytes leads to cytoskeletal damage, apoptosis, death
Specific treatments: Wash animal, NAC/SAM

44
Q

What are the sources, clinical signs, and diagnostic abnormalities for copper toxicity?

A

Sources: Pennies Dewormers, diet, genetic in dogs

CS: GI + LIVER + BLOOD, ACUTE-Vomiting, diarrhea, ulceration, pale MM, HEMOLYSIS/HEMOGLOBINURIA, ELEVATED LIVER ENZYMES.

CHRONIC (sheep)- Elevated liver enzymes, icterus, Hemolytic crisis (hemolysis + Methemoglobin), liver + kidney necrosis

Diagnostic Abnormalities: Hemoglobinuria, elevated liver enzymes, high copper levels/molybdenum

45
Q

What gene is mutated in dogs with copper sensitivity?

A

Commd1

46
Q

What type of signs are most common in sheep with copper toxicosis? Camelids?

A

Chronic. Chronic- Weeks/Months – most common in
sheep
* Elevated liver enzymes
* Icterus
* Hemolytic crisis -> Hemolysis. Methemoglobin
* Liver and kidney necrosis
In camelid species such as alpacas or llamas, no hemolytic crisis is seen, although extensive liver necrosis remains a consistent manifestation.

47
Q

What is the mechanism of action and specific treatments for copper?

A

MOA: Damage to liver, lysosome bursts, copper into blood, hemolytic crisis + ROS/oxidative damage
Specific treatments: Special diets with high molybdenum, chelation, REDUCE ABSORPTIONA ND ENHANCE ELIMINATION (Zinc acetate, Ammonium tetrathiomolybdate), Sodium thiosulfate, Antioxidants

48
Q

How is copper absorbed and secreted?

A

Absorbed in GI tract and EXCRETED IN BILE

49
Q

What are factors that increase sensitivity to copper toxicosis?

A

Low dietary intake of sulfur and molybdenum (help with excretion), sheep/jersey cattle, genetics in dogs, pastures with high copper content

50
Q

What are the sources, clinical signs, and diagnostic abnormalities for iron toxicity?

A

Sources: supplements, snail/slug bait, fertilizer, hand warmers.
CS: GI + LIVER or CNS phase 1: Vomiting, Hyporexia, diarrhea, phase 2: hypovolemic shock, liver failure
Diagnostic Abnormalities: Serum Fe high

51
Q

What is the mechanism of action and specific treatments for iron? Special considerations for treatment?

A

MOA: direct GI irritant, once serum carrying capacity reached, free iron is deposited in liver-> ROS, lipid peroxidation, mitochondrial poison, hemolysis. When serum iron > binding and storage capacity -> causes toxicity
Specific treatments: no activated charcoal, Milk of magnesia, Chelation with Deferoxamine if high dose, NAC/SAM, monitor 4-6 weeks. long recovery.

52
Q

What liver toxicants have specific treatments and what are they?

A

Acetaminophen- Cimetidine in dogs only to block formation of NAPQI, Methylene Blue
Iron- no activated charcoal, Milk of magnesia, Chelation, Deferoxamine if high dose
Copper- Special diets with high molybdenum, chelation, Zinc acetate, Ammonium tetrathiomolybdate, Sodium thiosulfate
Amanita mushrooms- Vitamin K

53
Q

What are the species specific differences in Acetaminophen, BG algae, copper?

A

Acetaminophen: Cats > Dogs, BG algae: dogs, and LA due to lifestyles, Copper: Sheep > others

54
Q

Name and list types of lilies as ‘true’ or not

A

True lilies are Lilium or Hemerocallis genera. Include day lily, easter lily, tiger lily, Asiatic lily.
Not true lilies: Peace lily, Cala lily, Lily of the valley

55
Q

What are the clinical signs and diagnostic abnormalities in true lily toxicity?

A

CS: KIDNEY early: vomiting, salivation, dehydration, lethargy later: PU/PD, azotemia, Anuric renal failure, death
Diagnostic abnormalities: Azotemia, hyperphosphatemia, hyperkalemia

56
Q

What is the mechanism of action and specific treatments for true lily toxicity?

A

MOA: renal tubular necrosis
Treatments: emesis, charcoal, fluids, dialysis

57
Q

What are the clinical signs and diagnostic abnormalities in lily of the valley toxicity?

A

CS: GI + HEART Vom/Diar, bleeding, arrhythmias, seizures
Diagnostic abnormalities: cardiac

58
Q

Toxicity from what 2 plants look alike and include cardiac signs?

A

Lily of the valley and Foxglove (Digitalis)

59
Q

What is the mechanism of action and specific treatments for lily of the valley toxicity?

A

MOA: Cardiac glycosides and saponins- GI irritants (concentrated in bulb)
Treatments: Induce emesis if early, activated charcoal, fluids, gastroprotectants , monitor cardiac function and seizures

60
Q

What should you know about Calla and Peace lily toxicity?

A

Insoluble calcium oxalate crystals. Pain, numbness, inflammation in dogs/cats. +/- swelling. Rinse mouth, milk, emesis, fluids, gastroprotectants, anti-inflammatories, O2 if swelling-> breathing issues

61
Q

What plants contain calcium oxalate crystals?

A

Caladium, Dieffenbachia, Peace lily, Cala lily, Philodendron

62
Q

What plants contain soluble calcium oxalate?

A

Oxalis including Shamrock, Sorrel, Rhubarb

63
Q

What are clinical signs of Oxalis toxicity? What species are we concerned about?

A

GI + KIDNEY GI signs, Hypocalcemia, tremors, acute renal failure. Toxic to SA. More common in grazing livestock.

64
Q

What is method of action in Oxalis toxicity? Treatment?

A

Soluble calcium oxalate absorbed from GI, bind Ca and Magnesium, precipitate in urine, kidney failure. Treatment: emesis, charcoal, fluids, monitor kidney function

65
Q

What should you know about hosta toxicity?

A

Saponins foam and paralyze the GI tract. GI and skin irritant. Toxic to dogs, cats, horses. Key sign is abdominal pain/bloating. Can treat with the usual + antihistamine.

66
Q

What should you know about Autumn Crocus toxicity? Signs? Toxin? MOA? Who is susceptible?

A

Different from spring variety. Toxin is colchicine alkaloid. Works by binding tubulin and interfering with mitosis. Affects GI + MULTI ORGAN. Immediate or delayed for days. GI, Bloody diarrhea, Liver damage, kidney damage, Respiratory failure, seizures, death. MILK is major excretory pathway. SA and LA.

67
Q

What are the toxins in Daffodil/amaryllis toxicity? What is MOA?

A

lycorine and insoluble calcium oxalate crystals. Lycorene is alkaloid and Ca oxalate crystals are irritant.

68
Q

What are the signs of Daffodil/amaryllis toxicity? Who is it toxic to?

A

GI + MULTI ORGAN rapid onset GI, Tremors, tachycardia, dermal irritation, respiratory signs from breathing bulb dust. Toxic to LA and SA.

69
Q

What is the toxin associated with Tulip toxicity? What is MOA?

A

Tulipalin A and B are toxins. MOA: inhibit protein synthesis.

70
Q

What are the signs of Tulip toxicity? Who is it toxic to? Signs are similar to what other plant?

A

GI + MULTI ORGAN. GI signs, convulsions, tachycardia, respiratory issues. Toxic to LA and SA. SIMILAR TO DAFFODIL TOXICITY

71
Q

What is toxin involved in Cycad palm toxicity? What part of the plant is most toxic?

A

Seeds are the most toxic. Very toxic! 1-2 seeds can be fatal. Cyasin is toxin- hepatotoxic and GI irritant + other neurotoxins.

72
Q

What are the clinical signs of Cycad palm toxicity? Prognosis? Who is it toxic to?

A

GI + LIVER + NEURO. GI signs, Neuro signs, liver failure (dark urine, PU/PD, icterus, bleeding issues) Guarded prognosis! Toxic to LA and SA.

73
Q

What is toxin involved in Avocado toxicity? What part of the plant is most toxic?

A

Toxin is Persin. Causes necrosis of myocardial tissue and mammary epithelium. Leaves, bark, skin, seed, fruit all toxic.

74
Q

What animals are sensitive to avocado toxicity? What are the signs?

A

Toxicity most common in birds and horses- cats/dogs more resistant. Seed is choke hazard/pancreatits hazard for dogs. GI + CARDIO BIRDS- super fast onset- inability to perch, neck edema, difficulty breathing, heart damage. Horses/Ruminants- Head/neck edema, heart failure, colic, MASTITIS.

75
Q

What type of toxin is in Azaleas? What type of signs does it cause?

A

Grayanotoxins. GI + CARDIO signs. Key = Hypotension, irregular HR, heart failure

76
Q

What type of toxin is in Hydrangeas? What type of signs does it cause? Specific treatment?

A

Cyanogenic glycoside. GI signs. Vitamin B12a, sodium thiosulfate, sodium nitrite (cyanide antagonists)

77
Q

What type of toxin is in Lantanas? What type of signs does it cause? What other routes other than ingested?

A

Lantadene A and B which are liver/gallbladder toxins. GI + LIVER. GI signs, photosensitivity, Rumen stasis, Liver failure via cholestasis. Can be chronic exposure with feed refusal, weight loss, liver failure. Also see signs after burning plants.

78
Q

What plants can cause mechanical injury?

A

Cocklebur, Cactus, Seeds with barbs, Grass awns.

79
Q

What are factors that increase likelihood of LA plant poisoning?

A

First grazing in spring, Limited desirable forage available, After herbicide application (makes more palatable), After nitrogen application (concentrated in plants), Yard waste consumed, animals unfamiliar to pasture, toxic plants in harvested feed (mixed in with hay)

80
Q

What LA poisonous plants cause sudden death?

A

Larkspur, Locoweed, Jimsonweed, White Snakeroot

81
Q

What LA poisonous plants cause Musculoskeletal signs?

A

White Snakeroot

82
Q

What LA poisonous plants cause Cardiovascular signs?

A

Yew

83
Q

What LA poisonous plants cause neurological signs?

A

Yellow star thistle, Jimsonweed/thornapple, Bracken Fern, Locoweed, deadly nightshade

84
Q

What LA poisonous plants cause Enzootic hematuria in cattle?

A

Bracken Fern

85
Q

What LA poisonous plants cause anemia/methemoglobinemia?

A

RED MAPLE

86
Q

What LA poisonous plants cause GI/Liver signs?

A

Panicum (Klein grass)

87
Q

What LA poisonous plants cause birth defects in lambs? General category?

A

STEROIDAL ALKALOIDS, VERATRUM (SKUNK CABBAGE, FALSE HELLEBORE), NIGHTSHADE

88
Q

What is the method of action of steroidal alkaloids? Clinical signs? Examples of plants?

A

INHIBIT CHOLINESTERASE, PARASYMPATHOMIMETICS, INCREASE GI MOTILITY. BIRTH DEFECTS.

89
Q

What is important about Larkspurs?

A

Block NMJ, skeletal muscle paralysis, rapid death, cows most sensitive, sheep less sensitive.

90
Q

What is important about Yew?

A

Toxin is Taxine alkaloid. Block membrane Na+ transport -> depress myocardial conduction -> sudden collapse/death. Very deadly, esp to horses.

91
Q

What is important about Locoweed?

A

Depressed but nervous, react unpredictably, metabolic, CNS, cardio signs. Horses, high-altitude cattle dz.

92
Q

What is important about Yellow Star Thistle?

A

Contains neurotoxins, causes dysphagia due to dystonia of lips/tongue (loss of UMN inhibition), NIGROPALLIDAL MALACIA.

93
Q

What is important about Red Maple?

A

Hemolytic toxin. Hemolytic anemia, hemoglobinuria, Heinz body formation, icterus, death. Horses only, only wilted leaves.

94
Q

What is important about Veratrum?

A

Skunk cabbage/false hellebore. Inhibit cholinesterase, parasympathomimetic, Gi motility, hypotension, birth defects if ewes consume in first trimester. Same group as nightshades/tomatoes.

95
Q

What is important about Nightshade?

A

Tropane alkaloid, same group as Jimsonweed. Atropine, blocks acetylcholine at muscarinic receptors, Ileus, tachycardia, mydriasis, delirium.

96
Q

What is important about Bracken Fern?

A

Contains toxic glycoside that alkylates DNA -> bone marrow suppression and carcinogenic. Bladder neoplasia, hemorrhages. Cattle Enzootic Hematuria. Young fiddleheads 5 x toxic, cows like them.

97
Q

What is important about Jimsonweed?

A

Tropane alkaloid, same group as Belladonna/deadly nightshade. Atropine, blocks acetylcholine at muscarinic receptors, Ileus, tachycardia, mydriasis, delirium.

98
Q

What is important about Black Walnut?

A

Shavings are toxic. Causes laminitis in horses. Toxin is a quinone.

99
Q

What is important about Staggers?

A

Caused by grasses. Grassland staggers caused by tremorgenic mycotoxins. When stimulated, spastic gait, spasms, seizures. Canary grass, Bermuda grass, Ryegrass, Dallis grass

100
Q

What is important about Choke Cherry (Prunus)?

A

Cyanogenic glycosides. Cyanide released by plant. Blocks Hb from releasing O2 to tissues. Cherry red blood, sudden death.

101
Q

What is important about White Snakeroot?

A

Cardiac and skeletal muscle degeneration/necrosis, ketosis, excreted rapidly in milk- protects animal.

102
Q

Which is more toxic to a cow nitrate or nitrite? Would you worry about ingestion of both?

A

Nitrite is much more toxic. Nitrate is still a problem for ruminants because nitrate is reduced to nitrite in the rumen and is very toxic. But they can acclimate to high-nitrate forages.

103
Q

What are some highly toxic plants found in Wisconsin?

A

Choke cherry, Cocklebur, Jimsonweed, Poison hemlock, Red maple (horses only), white snakeroot

Toxicology (1 decks)

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