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Toxicology > Final Exam > Flashcards

Final Exam Flashcards

1
Q

What mycotoxins are associated with moldy nuts/cream/cheesecake?

What mycotoxin is often found in grass?

MoA of these?

What species are most sensitive?

Early effects? High dose effects?

Cause of death?

What is the prognosis dependent on?

A

Penitrem A

Rocquefortine

Inhibits glycine & GABA –> promotes presynaptic ACh release

Dogs & Cats

Acute onset of tremors, Death

Muscle contractions inhibit respiratory muscles

Prognosis depends on if animal responds to anticonvulsant therapy, otherwise resp. failure = death

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2
Q

Which mushroom is responsible for the most fatal mushroom poisonings in animals & humans?

3 phases of this mushroom toxicity?

A

Amanita mushrooms (Amanita spp.)

Gastroenteritis phase (up to 24hrs): vomiting, hemorrhagic diarrhea

Latent Phase (12-24hrs): improvement of GI signs, early signs of kidney failure (elevated enzymes)

Liver & Kidney failure: neurologic dysfunction, death 3-7 days post ingestion of mushrooms

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3
Q

Tx for amanita toxicity?

A

emesis, gastric lavage, activated charcoal, fluid therapy, supportive care

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4
Q

What mycotoxin is responsible for “black patch disease” and a “slobber factor” in horses?

What plant should you be on the lookout for on pasture?

A

Slaframine metabolites (from Rhizoctonia leguminicola)

Moldy red clover

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5
Q

What effects do Tall Fescue & Anual Ryegrass have?

What toxins are produced?

MoA?

A

Poor performance, peripheral vasoconstriction causing heat intolerance (loss of temp control) & necrosis of extremities –> economic losses

Ergot alkaloids & ergoline alkaloids

Interacts with adrenergic receptors especially dopaminergic & alpha-1 receptors (vasoconstriction, reduced prolactin secretion, altered gut motility, impaired ability to adapt to seasonal changes)

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6
Q

Clinical Picture of Fescue toxicosis?

What breed of cattle is more susceptible to Fescue Foot?

What part of the plant is the toxin sequestered in?

Tx?

A

Poor feed & growth conversion, reduced milk yield, retained winter coats, poor fertility (permanent), heat intolerance, necrosis of extremities, more severe during cold weather, prolonged gestation in mares

Brahman cattle

Seed heads

Remove source, nutrient supplementation, metoclopramide (dopamine blocker, but BANNED in animals intended for consumption), domperidone for horses to alleviate agalactia

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7
Q

What plants produce Tremorgens?

How soon do you see signs? Clinical Pic?

Tx?

A

Perennial ryegrass (most important!), Dallis grass, Bermuda grass

Within 7 days of exposure: fine tremors progressing to ataxia, hypermetria, seizures, usually after animal becomes excited

No specific treatment, self-resolving once plants are removed

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8
Q

What plants produce Indolizidine alkaloids?

Toxin that is produced? Effects?

A

Locoweeds

Swainsonine: alpha-mannosidosis (lysosomal storage disease - sugars don’t get broken down and accumulate), locoism, repro failure, ill-thrift, causes a general dysfunction of CNS & endocrine effects

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9
Q

What organism produces swainsonine in locoweeds?

Why do we have to be worried about this toxin even if animal is exposed to low amounts?

T/F: we are more concerned with the mother who is being directly exposed than a nursing calf

A

Endophytes

Exposure can be cumulative

False: toxin is readily passed in milk

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10
Q

Clin Pic for swainsonine toxicosis in cattle and horses?

Effects when there is fetal exposure?

A

Locoism (sensory & motor dysfunction), infertility or subfertility in males & females:

Cattle: low carriage of head, vacant stare, head trembling, difficulty eating

Horses: listless, easily exciteable, stumble when stimulated, fall over backwards when rearing, unpredictable and PERMANENTLY unsafe to ride (must advise clients to not ride horses exposed to locoweed)

Fetal exposure: arthrogryposis, abortions, weak young

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11
Q

What clin path data may indicate swainsonine toxicosis?

Histopath findings?

Tx?

A

decreased serum alpha-mannosidase, decreased serum protein & albumin, decreased thyroid hormones, increased liver enzymes

Vacuolated cells

Tx: no effective tx, remove source of exposure, recovery is slow

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12
Q

Which metals are we most concerned about in veterinary medicine?

A

Lead, copper, zinc, sodium, iron, arsenic (metalloid, not a true metal)

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13
Q

NOAEL for lead in people?

Major effects of lead poisoning?

Environmental concerns?

Acidic/Basic environment = more absorption of lead?

Of blood, liver/kidney, brain, bone, in which tissue does lead have the highest half-life?

A

There is none, no exposure is safe

Nervous system (decrease IQ), mild GI (green diarrhea in birds), anemia

Lead does not breakdown so removal of it is needed to eliminate exposure,

Acidic

Bone (1000 days): most lead becomes sequestered here (lead follows calcium)

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14
Q

Most prominent effects of lead poisoning?

A

CNS effects: stupor, convulsions, depression, anorexia, blindness, acute death (extreme exposure), apparent blindness with absence of ocular lesions (cattle)

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15
Q

Diagnosis for lead poisoning?

Tx?

Best chelator for large animals? Why?

Best chelator for general use?

A

Whole blood (heparinized, fresh) sent to lab, liver/kidney samples of dead animals, ALAD suppression, lead line on developing bone

Tx: remove source (retained lead in body, any exposure in environment), corticosteroids/edema for brain edema, supportive care, sulfate salts may reduce absorption???

EDTA (cheap) either via slow IV or IM, BID, 3-5 days

Dimercaperol (BAL) - better at removing lead from brain, can be combined with EDTA, IM, can give to birds

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16
Q

What metal are sheep & goats most susceptible to?

Characteristic lesion?

Common way for sheep to be accidentally exposed to excess copper?

A

Copper

gun-metal black kidneys

Sheep fed cattle feed (amt of Cu in cattle feed too high for sheep) or exposure to algaecides containing copper

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17
Q

MoA for copper toxicosis in sheep?

Initial signs of copper toxicity?

Postmortem signs?

What sample(s) should you send for necropsy? Why?

A

Copper uptake via hepatocytes and accumulation until some stressful event that results in massive Cu release into blood –> oxidative damage to RBC’s & hemolysis

Dead sheep, icterus, GI irritation with acute exposure

Pronounced icterus, brown blood, swollen/pale/friable liver, black kidneys

Liver AND kidney - liver Cu levels can be lower following acute phase and sending liver only can result in an incorrect diagnosis

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18
Q

Appropriate Cu levels in feed for sheep?

Appropriate Cu:Mo for sheep?

What can happen if Mo is to low?

Chelator for copper?

Other Tx for Cu toxicity?

A

20ppm

Between 6:1 & 10:1

Induce a copper toxicity even if Cu levels are appropriate

Penicillamine

Ammonium tetrathiomolybdate & oral ammonium molybdate

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19
Q

What happens in Molybdenum “poisoning”?

A

Excess Mo can induce Cu deficiency –> reduction in growth & production, lightening of coat color, reduced fertility, lightening of coat color, immune suppression,

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20
Q

How may a dog get a zinc poisoning?

What may happen in a dog at a higher incidence in zinc poisoning? In other species?

Clinical pic?

A

Ingestion of zinc pennies

Hemolytic anemia due to oxidative damage, pancreatitis in other species

Clin Pic: vomiting & diarrhea +/- blood, hemolytic anemia several hours to days later, +/- icterus, anorexia colic, pancreatitis

21
Q

Tx for Zinc poisoning?

A

Antacids to increase gastric pH (reduce Zn dissolution), remove source (surgery, endoscopy), chelation (Ca-EDTA, Succimer), supportive care

22
Q

Pathologic consequences of sodium poisoning (water deprivation)

Clinical Picture?

Post mortem findings?

A

Brain edema & eosinophilic meningoencephalitis

Clin pic: acute & rapid progression, restlessness, circling, ataxia, head pressing, blindness, muscle tremors, dog-sitting position, seizures, respiratory failure, progression faster in swine than in cattle

Cortical & cerebral edema, eosinophilic meningoencephalitis (perivascular cuffing), neuronal degeneration

23
Q

Tx for salt poisoning?

A

SLOW rehydration - oral guideline (2ml water/kg/hr in small divided doses), slow IV alternatively given with furosemide, mannitol diuresis may reduce brain edema

24
Q

3 main organ systems affected by iron poisoning?

MoA?

A

GIT, heart, liver

Elemental iron is corrosive to GI mucosa, excess iron results in unbound iron (normally bound to transferrin) and subsequent free radical mediated oxidative damage to tissues (liver and myocardium most susceptible), coagulopathies, lactic acidosis can occur (excess iron forces non-oxidative ATP production)

25
Q

Clinical picture for Iron toxicosis?

Postmortem findings?

A

Early (1-6 hrs): vomiting & diarrhea (+/-blood), –> latent phase & apparent recovery –> after 6-24 hrs heart failure, liver failure, acidosis, seizures, coma, death –> if survives, can have GI scarring & strictures

PM: gastric ulceration & edema, yellow/brown discoloration around injection sites, swollen liver, dark kidneys, hepatosis,

26
Q

What is a good sample to analyze for signs of arsenic poisoning?

MoA?

Clin Pic?

A

Hair (arsenic tends to accumulate here)

Extreme GIT irritation & contact necrosis: tissue sloughing, ulceration, hemorrhage, increased fluid secretion,

Clin pic: vomiting & Diarrhea +/- blood. dehydration, shock

27
Q

Common pesticides seen in animal poisonings?

What makes a good pesticide?

Most common source?

Are delayed neuropathies seen more in organophoshates or carbamates

A

Anticholinesterases (OP/scarbs), pyrethrins/pyrethroids, anticoagulants

High potency, hard to detect

Agricultural products

Organophosphates

28
Q

Clinical picture of pesticide

Diagnosis of Anticholinesterase poisoning?

T/F: delayed assays are quite useful for carbamates

A

Rapid progression: salivation, vomiting, diarrhea, dyspnea, muscle tremors, paresis, paralysis, seizures, respiratory muscle failure,

ChE inhibition in serum/whole blood (alive animals), ChE inhibition in brain (dead animals)

False, they are NOT useful

29
Q

Key to pesticide poisoning? (anticholinesterase)

In dogs, ? is given to counter nicotinic or cholinergic effects?

In cattle, ? is given to counter nicotinic or cholinergic effects that kill them?

2-PAM is only useful for OP or Carbamate poisoning?

A

EARLY treatment, removal of source, high doses of activated charcoal

Atropine, cholinergic

Activated Charcoal, Nicotinic

OP

30
Q

What is the most widely used pesticide, especially in household scenarios have replaced OP’s as a less toxic alternative?

Type of tissues that pyrethroids like to accumulate in?
What is the concern here?

Clinical pic?

A

Pyrethrins & pyrethroids

They are lipophilic - so fat tissue, skin; at multiple high doses, instead of fat acting as a reservoir and slowly being released, the distribution into blood becomes dependant on fat dude to slow absorption

Clin Pic: salivation (lack of swallowing), hyperaesthesia (dermal sensitivity), ear twitching/tail flicking/???

31
Q

Tx for Permethrin/Pyrethroid toxicity?

A

Decontaminate with mild dishwashing DETERGENT (don’t use plain water or it will drive toxin deeper into skin), activated charcoal, diazepam (mild neuro effects), methocarbamol (moderate neuro), phenobarb (severe neuro),

32
Q

Duration of action of 1st generation anticoagulants? Why?

Duration of 2nd generation? Why?

Which clotting factors require vitamin K for activation?

How do anticoagulants interfere with clotting?

What kind of drugs can suppress liver metabolism and what does this do to effects of anticoagulants?

A

Short, short half-lives, effects last a few days

Long, long half-lives, effects for 12-30 days

Clotting factors II, VII, IX, X

Interfere with vitamin K1 recycling in intrinsic, extrinsic, and common clotting pathways

Cimetidine, sulfonamides, fluconazole, phenylbutazone - increase duration of effects of anticoagulants

33
Q

Clinical picture for anticoagulant poisoning?

Tx?

A

Initial signs are generally non-specific: lethargy, depression, pallor, or even death, paw swelling (bleeding subcutaneously); lameness, anemia,

Tx: decontamination, vitamin K supplementation, blood transfusions,

34
Q

MoA for strychnine poisoning?

Tx?

What is prognosis dependent on?

A

blocks effect of glycine on inhibitory GABA receptors –> suppresses chloride conductance –> muscle spasms –> extension of limbs –> tonic convulsions

Tx: need to do supportive care ASAP (life-saving!), decontaminate (emesis, gastric lavage, activated charcoal, cathartics), control muscle spasms (phenobarb, diazepam, methocarbamol), IV fluids, control hyperthermia/acidosis/hypoxia,

How soon Tx is given, control of seizures, maintenance of respiration

35
Q

MoA of Zinc Phosphide?

A

Corrosive, hemorrhagic gastroenteritis, reacts with stomach acid to form phosphine gas (rapidly absorbed, cytotoxic, general organ failure - heart, brain, liver, kidney, lung, most vulnerable)

36
Q

MoA of Bromethalin

High dose effects?

Low dose effects?

Low dose or high dose poisoning more common?

A

mitochondrial??

Excitatory syndrome, tremors, seizures, death

Paralytic syndrome: progressive CNS depression –> hind limb weakness –> paralysis –> forelimb weakness –>coma

Low dose (paralytic)

37
Q

Signs of mold growth?

What does mycotoxin production depend on?

Difference between action levels & guidance/advisory levels?

A

Heat, smell, caking/clumping, discoloration, slow movement out of bins

Genetic potential, environmental conditions (generally warm & humid), growth stage/proliferation

Action levels must be reported to FDA if action levels are exceeded (violative)

Guidance or Advisory levels provide an adequate margin of safety and are not subject to enforcement by the FDA

38
Q

What is the most prominent genus of fungus for each listed mycotoxin? Hint: some fungi may be responsible for more than 1 mycotoxin group

Aflatoxins, zearalenone, trichothecenes, ochratoxins, fumonisins

A

Aflatoxins: Aspergillus spp.

Ochratoxins: Penicillium/Aspergillus spp.

Fumonisins: Fusarium spp.

Trichothecenes: Fusarium/Stachybotrys spp.

Zearalenone: Fusarium spp.

39
Q

What foods/feeds are aflatoxins commonly associated with?

Aflatoxin contamination is slow/rapid?

What is it about aflatoxins that increases their risk of exposure to human/animal consumption?

Of the types of Aflatoxins (AB1, AB2, AG1, AG2, AM1, AM2), which ones are associated with milk and how are they formed?

A

Seed crops, oilseeds, spices, nuts

Rapid (high levels within 2-7 days of inoculation)

Persistent toxin that can survive food processing

AM1 & AM 2 associated with milk, they are metabolites of AB1 & AB2

40
Q

Why are we worried about Aflatoxins?

Action levels (ppb) in corn/grains meant for immature animals/dairy/unknown destination, breeding stock/mature poultry, finishing swine, finishing beef cattle/cottonseed meal, all other animal feeds?

Action level for milk meant for human consumption?

A

Potent carcinogens & hepatotoxic

20 ppb for corn/grains meant for immature animals/dairy/unknown destination

100 ppb for breeding stock/mature poultry

200 ppb for finishing swine

300 ppb for finishing beef cattle/cottonseed meal

20 ppb for corn/grains for all other animal feeds

0.5 ppb

41
Q

Tx for Aflatoxin toxicosis?

Prognosis?

A

Remove source, supportive care, provide good nutrition

Guarded: liver’a return to normal function may be delayed

42
Q

What kinds of foods are we concerned about with Ochratoxins?

Ochratoxin ? is most common

What other mycotoxin causes an identical syndrome?

Why are we concerned with Ochratoxin?

What is the current action level for Ochratoxin in food?

A

Mainly cereals, but also beans (& coffee beans), dried fruit, wine

Ochratoxin A!

Citrinin

Nephrotoxic (chronic renal failure is typical), teratogenic, carcinogenic, gastroenteritis

There is no action or advisory level currently

43
Q

Tx for ochratoxin?

A

AC if given early, supportive treatment (esp. for kidney failure), vitamin C for can help with egg laying production problems in hens

44
Q

What food are fumonisins most commonly found in?

Is Fumonisin B1, B2, or B3 the most common?

What pathology does this toxin cause in horses? Pigs?

What effects does it have across all species at high dosages?

A

corn

Fumonisin B1

Horses: Leucoencephalomalacia (LEM) - neurological syndrome most common, sometimes with hepatic failure

Pigs: pulmonary edema - consistently develops 3-6 days after initial exposure, rapid progression –> death within hrs of onset of dyspnea

Hepatotoxic & nephrotoxic

45
Q

How much ppm of fumonisin can be allowed in the diet of equids & rabbits?

For swine & catfish?

Tx?

Prognosis?

A

No more than 20% of diet may have >5ppm

No more than 50% of diet may have >20 ppm

Tx: remove source, supportive care, +/- AC

Poor prognosis due to relatively rapid progression of signs

46
Q

Which mycotoxin is associated with grains in cool, wet weather and in late-harvested/overwintered grain?

What is the main toxin formed by these compounds?

Main effects of the toxin?

When will you see vomiting?

Tx?

A

Trichothecenes

Deoxynivalenol (DON aka vomitoxin)

Effects: feed refusal –> off-feed, radiomimetic (bone marrow suppression), necrotic oral & skin lesions of the head (swine & poultry)

If animal is forced to keep on eating feed containing vomitoxin, then will eventually see vomiting

Tx: gradual recovery in 1-2 weeks, no specific Tx

47
Q

Advisory level for DON for finished wheat products that may be potentially consumed by humans

Advisory level for DON for ruminating beef & feedlot cattle older than 4 months and ruminating dairy cattle older than 4 months on grains & grain by-products

A

1 ppm

10 ppm

48
Q

What estrogenic mycotoxin is mostly associated with corn?

What kind of animal is most susceptible to effects?
What are the effects?

A

Zearalenone

Prepubertal gilts

non-standing heat, infertility, abortion, vulvovaginitis –. which can lead to prolapse (vaginal or rectal)

49
Q

Tx for Zearalenone toxicosis?

Action/advisory level?

A

Remove source, treat any prolapse, symptomatic treatment - good/fair prognosis

None

Toxicology (3 decks)

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