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SS - Exam 1 > Toxicology 1 > Flashcards

Toxicology 1 Flashcards

1
Q

Sodium toxicosis /water deprivation

A

Combo of water volume depletion (LA) and ingestion of excess salt (SA)
Excess could be play dough, road salt/melt run off, frozen over water sources

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2
Q

acute toxicity - sodium toxicosis

A

Salt ingestion or activated charcoal overuse
Passive movement of Na+ across BBB due to increased Na+ levels. Inhibition of energy production (glycosis) necessary for active transport to excrete Na from CNS - water replacement - primary effect is cerebral edema

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3
Q

Chronic toxicity - water deprivation

A

Water deprivation ≥ 3 days
Generation of idiogeneic, organic & inorganic osmoses in CSF to compensate for increased osmalolity in blood
Rapid water replacement = dilution of Na+ concentration in blood = movement of water into CNS = cerebral edema

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4
Q

Diagnosing sodium toxicosis /water deprivation

A

> 170 mEa/L Na in serum or CSF
1800 ppm Na in brain
Laminar necrosis in brain in all animals - eosinophilic cuffing in swine only

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5
Q

Clinical signs of water deprivation in cattle

A

GIT irritation, anorexia, nasal discharge, thirst polyuria, rumen stasis, diarrhea, mucus covered feces, paresis/rear leg knuckling, blindness, nystagmus, belligerent, seizures

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6
Q

NaCL toxicity

A

Cattle, swine & horses -
Dogs
Poultry

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7
Q

Clinical signs in swine

A

Onset time ≥ 3 days
Dog sitting, wandering, pivoting around foot
Blind, deaf, nose twitching, seizures, coma, anorexia, constipation
*star gazing, *jaw champing, head pressing, pruritus
Eosinophilic perivascular cuffing in brain with laminar necrosis

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8
Q

Clinical signs in poultry

A

Takes 1-2 days no water = sodium toxicosis
Depression, lethargy, anorexia, thirst, diarrhea, nasal discharge, dyspnea, nervousness, paresis, serisures

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9
Q

Lesions in poultry sodium toxicosis

A

Enteritis, ascites, generalized edema, hydro-pericardium

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10
Q

Clinical signs in dogs

A

<4 hours from acute ingestion

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11
Q

Treating swine or cattle with Na toxicosis

A

Give access to small amounts of water in 1 hour intervals
Prognosis is very poor

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12
Q

Treatment for dogs with Na toxicosis

A

Replace free water deficit
Consider use of furosemide - loop diuretic for Na excretion
Difficult therapy bc of intracellular dehydration combined w hypervolemia, monitor Na levels, monitor pulmonary edema

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13
Q

Ionophores

A

Indirect neurotoxic feed additive (muscular toxicosis)
- monensin, salinmycin, iasalocid - coccidiostatic feed antiviral & growth promotants

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14
Q

Ionophore toxicity

A

Primarily a problem in horses, sheep & turkeys
Horses & turkeys have lower LD50 for monensin than cattle & chickens - death can be sudden

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15
Q

Mechanism of Ionophore toxicity

A

Toxic action related to influx of ions across mitochondrial membranes of heart & skeletal muscle - intracellular Ca2+ accumulation - opening of MPTP (mitochondrial permeability transition pore) - decrease ATP formation & cell necrosis = cell death

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16
Q

Organ failure in horses & cats

A

Heart > skeletal muscle

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17
Q

Organ failure for cattle & rabbits

A

Heart = skeletal muscle

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18
Q

Organ failure for sheep, pigs, dogs

A

Skeletal muscle > heart

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19
Q

diagnosing Ionophore toxicity

A

Anorexia, GIT problems, death following use of new concentrate or minerals
- Se deficiency, cardiac infarct, cardio toxic plants

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20
Q

Lesions for Ionophore toxicity

A

Pale, flabby heart & skeletal muscles, hydrothorax, ascites necrosis / white streaking of skeletal &/or heart muscles

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21
Q

Treatment for Ionophore toxicity

A

Change feed immediately
There’s no treatment for horses
Prognosis is guarded to poor

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22
Q

Yellow buckeye toxicity

A

Aesuculus flava
All parts are toxic but fruiting /nut are most toxic
Toxic principle - aesculin

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23
Q

Clinical signs for buckeye toxicity

A

Ataxia, muscle tremors, lateral recumbency, paralysis, in coordination w hypermetria (high stepping) hyperesthsia, nystagmus/strabismus, prostration, seizures, coma

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24
Q

Lesions and treatment for buckeye toxicity

A

No lesions just presence of Buckeyes in rumen
Sedatives until symptoms resolves
Decontamination

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25
Q

Indole alkaloids - claviceps ergot

A

Structures formed from group of fungi in genus claviceps
Fungi infect flowering plants
Sclerotia - dark purple, brown or black & resemble seed heads

26
Q

Toxicity of claviceps

A

Produce mixture of ergot peptide alkaloids (ergotamine, ergo sine, ergocyptine, ergocristine, ergonovine) similar structure to LSD

27
Q

Mechanism of action of ergotamine

A

CNS properties similarly to LSD, vasoconstriction - burning sensation with subsequent gangrene
Decreased production of prolactin in reproductive females

28
Q

Clinical signs for acute ergotism

A

Onset 1-5 days (course 1-7 days)
Ataxia, hyperexcitable, muscle tremors, seizures, opisthotonus (clin signs will subside if leave animal alone)
Syndrome is inseparable from Bermuda grass staggers & perineal ryegrass staggers

29
Q

Chronic clinical signs for ergotism

A

Onset 1 week
Anxious, lame, rising temp/pulse/resp rate (TRP)
Swelling above coronary band, ataxic, feed refusal
Sloughing of hooves, ears, tail, skin, teats
- necrosis on tip of tongue in sheep
- potential abortion

30
Q

Clinical signs for swine - claviceps

A

(Reproductive)
Onset in late gestation (last 2-4 wks)
Chronic effect, similar to fescue in mares (decreased prolactin)
Feed refusal, agalactia, gestation shorted by 3-5 days, abortion is rare

31
Q

Fescue, source & toxicity

A

Lolium arundinaceu, >95% infested with endophytic fungus
All parts of plants infected with endophyte & ergot alkaloids
Primary toxin - Ergovaline
Toxicosis primarily in cattle & mares

32
Q

Mechanism of action for fescue

A

Ergot alkaloids have multiple physiologic effects
D2 dopaminergic (decreased prolactin) and alpha 1 agonist (vasoconstriction)
4 primary syndromes
- reproductive dysfunction
- summer slump: intolerance to heat
- fescue foot - peripheral vasoconstriction w gangrenous necrosis
- fat necrosis - abdominal

33
Q

Bromethalin rodenticide

A

Rodenticide - often contain 0.01% bromethalin

34
Q

LD50 for cats

A

0.54mg/kg
MLD - 0.45mg/kg
MTD - 0.3mg/kg

35
Q

LD50 for dogs

A

3.7mg/kg
MLD - 2.5 mg/kg
MTD - 1.67mg/kg

36
Q

Mechanism of action for bromethalin toxicity

A

Metabolized in the body, metabolite uncouples oxidative phosphorylation esp in brain
Lack of ATP production = weak Na/K gradient pump in brain = fluid accumulates in myelin sheaths = inference of axon transmission = respiratory arrest/paralysis
Myelin edema appears like spongiosis

37
Q

Clinical signs for bromethalin toxicity - acute

A

Acute/convulsant syndrome
Dose ≥. LD50
Can appear 10-24 hr post ingestion
Mortality rate ~ 100%
Agitation, muscle tremors, hyperesthsia, hyperthermia, unequal pupil size, focal, generalized seizures, death
Lesion: spongiosis

38
Q

Clinical signs for chronic brothemalin toxicity

A

Paralytic syndrome
Delay in signs usually occur 2 to 5 days post ingestion
Tremors, ataxia, CNS depression, recumbancy, anisocoria, lateral recumbency
Hind limb paresis, loss of deep pain
Lesions: white matter spongiosis

39
Q

Diagnosing bromethalin toxicity

A

Diagnosing possible exposure rate
Clinical signs
Ante-mortem fat biopsy
Post-mortem analysis of fat, liver, kidney

40
Q

Treating & prognosis bromethalin toxicosis

A

Decontamination - Emesis & repeated doses of activated charcoal (which undergoes enterohepatic recirculation 48hrs)
Treat seizures/supportive care
Prognosis varies on signs, amt ingested and reaction from treatment

41
Q

Mycotoxins

A

Fumoisin, slaframine, penitrem A & roquefortine
Molds or fungi developed in feed or silage during storage
≤13.5% moisture

42
Q

Fumonisin

A

Moldy corn poisoning
Fusarium fungi especially back in horses
Most cases appear between December-January

43
Q

Toxicity of fumonisin

A

B1 & B2 - interfere with formation of sphingolipids, cell membrane and lipid rich structure formations
Low morbidity, high case mortality

44
Q

Fumonisin mechanism of action

A

Interferes with sphingolipid biosynthesis - increased sphingosine - inhibition of L-type calcium channels - decrease of Ca2+ release from myocardial sarcoplasmic reticulum - decreased contractility - left sided heart failure

45
Q

Clinical signs in horses w fumonisin toxicity

A

Onset 1-4 wks
Acute/rapid CNS clinical signs, death 4-12 hours following onset. Liver/cardiac disease 3-8 days
CNS: depression, ataxia, blindness, facial paralysis, head pressing, maniacal behavior, hypersensitivity, convulsions
Liver tox: mastication problems, yawning, icterus, head edema, petechial hemorrhage

46
Q

Diagnosing and treating fumonisin toxicity

A

Presence of contaminated feed & clinical signs
Necropsy - lesion: malacia /necrosis of white matter of brain + hemorrhage
Treatment: remove corn from diet

47
Q

Slaframine

A

Slobber syndrome - grown on legumes or clover/alfalfa
Common in horses, goats, cattle, sheep
High morbidity / low mortality

48
Q

Mechanisms of action for slaframine

A

Metabolized in liver to ketoimine (active metabolite)
The amine structure in ketoimine has quarternary amine structure similar to acetylcholine and is a parasympathetic alkaloid that works on cholinergic receptors
Does not cross BBB

49
Q

Clinical signs of slaframine toxicity

A

SLUD: hypersalavation, lacrimation, urination, diarrhea, dyspnea, feed refusal, piloerection, bloat
- rare abortions/death

50
Q

Treatment /prevention of slaframine toxicity

A

Usually none
Antihistamines
Avoid buying legume hay after second cutting or in a wet growing year
Avoid atropine in horses

51
Q

Tremorgenic mycotoxins

A

(Aspergillus & penicillium)
Produce molds that grow in organic, decaying matter (milk, moldy English & black walnuts) commonly found in garbage, compost piles, road-kill
Harbor endotoxins/enterotoxins

52
Q

Toxicity of tremorgenic

A

Dogs -
Penitrem A & roquefortine are lipophilic, preformed (no metabolizing) = rapid onset & enteroheptic recirculation
*toxic to all species of animals

53
Q

Mechanism of action of tremorgenic toxins

A

Suspected they affect transmission of impulses across motor end plates
± inhibits inhibitory neurotransmitters
± increases release of excitatory neurotransmitters

54
Q

Acute clinical signs of tremorgenic toxins

A

Onset 10min-4hrs, course 2-3 days
Vomiting, decontamination, salivation, ataxia, muscle tremors, hyperesthesia, facial twitching, clonic-tonic seizures, paralysis, nystagmus

55
Q

Diagnosing /treating tremorgenic toxins

A

Stomach contents analysis
Differentiate from strychnine or ethylene glycol toxicity**
Treat: diazepam ± effective, activated charcoal

56
Q

Toxins causing toxicity with tremorgenic toxins

A

Lolitrems A & B in perennial rye grass
Paspalitrems in Bermuda & Dallis grass
Fumitremorgens in ergot sclerotia

57
Q

Chronic clinical signs of tremorgenic toxins

A

Onset 7-10 days - moderate morbidity, low mortality
Muscle tremors, paralysis, nystagmus/anisocoria, hypersalavation, vomiting, ataxia, hypermetria, hyperesthesia

58
Q

Diagnosing /treating tremorgenic toxins

A

Feed analysis, field assessment, ergot sclerotia in hay assessment
Change feed/remove toxins
Sedate animals as needed to protect from CNS signs

59
Q

Endotoxins cause

A

Inflammatory reaction

60
Q

Enterotoxins cause

A

Fluid and electrolyte loss

SS - Exam 1 (33 decks)

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