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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
Indole alkaloids - claviceps ergot
Structures formed from group of fungi in genus claviceps Fungi infect flowering plants Sclerotia - dark purple, brown or black & resemble seed heads
26
Toxicity of claviceps
Produce mixture of ergot peptide alkaloids (ergotamine, ergo sine, ergocyptine, ergocristine, ergonovine) similar structure to LSD
27
Mechanism of action of ergotamine
CNS properties similarly to LSD, vasoconstriction - burning sensation with subsequent gangrene Decreased production of prolactin in reproductive females
28
Clinical signs for acute ergotism
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
Chronic clinical signs for ergotism
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
Clinical signs for swine - claviceps
(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
Fescue, source & toxicity
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
Mechanism of action for fescue
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
Bromethalin rodenticide
Rodenticide - often contain 0.01% bromethalin
34
LD50 for cats
0.54mg/kg MLD - 0.45mg/kg MTD - 0.3mg/kg
35
LD50 for dogs
3.7mg/kg MLD - 2.5 mg/kg MTD - 1.67mg/kg
36
Mechanism of action for bromethalin toxicity
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
Clinical signs for bromethalin toxicity - acute
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
Clinical signs for chronic brothemalin toxicity
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
Diagnosing bromethalin toxicity
Diagnosing possible exposure rate Clinical signs Ante-mortem fat biopsy Post-mortem analysis of fat, liver, kidney
40
Treating & prognosis bromethalin toxicosis
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
Mycotoxins
Fumoisin, slaframine, penitrem A & roquefortine Molds or fungi developed in feed or silage during storage ≤13.5% moisture
42
Fumonisin
Moldy corn poisoning Fusarium fungi especially back in horses Most cases appear between December-January
43
Toxicity of fumonisin
B1 & B2 - interfere with formation of sphingolipids, cell membrane and lipid rich structure formations Low morbidity, high case mortality
44
Fumonisin mechanism of action
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
Clinical signs in horses w fumonisin toxicity
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
Diagnosing and treating fumonisin toxicity
Presence of contaminated feed & clinical signs Necropsy - lesion: malacia /necrosis of white matter of brain + hemorrhage Treatment: remove corn from diet
47
Slaframine
Slobber syndrome - grown on legumes or clover/alfalfa Common in horses, goats, cattle, sheep High morbidity / low mortality
48
Mechanisms of action for slaframine
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
Clinical signs of slaframine toxicity
SLUD: hypersalavation, lacrimation, urination, diarrhea, dyspnea, feed refusal, piloerection, bloat - rare abortions/death
50
Treatment /prevention of slaframine toxicity
Usually none Antihistamines Avoid buying legume hay after second cutting or in a wet growing year Avoid atropine in horses
51
Tremorgenic mycotoxins
(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
Toxicity of tremorgenic
Dogs - Penitrem A & roquefortine are lipophilic, preformed (no metabolizing) = rapid onset & enteroheptic recirculation *toxic to all species of animals
53
Mechanism of action of tremorgenic toxins
Suspected they affect transmission of impulses across motor end plates ± inhibits inhibitory neurotransmitters ± increases release of excitatory neurotransmitters
54
Acute clinical signs of tremorgenic toxins
Onset 10min-4hrs, course 2-3 days Vomiting, decontamination, salivation, ataxia, muscle tremors, hyperesthesia, facial twitching, clonic-tonic seizures, paralysis, nystagmus
55
Diagnosing /treating tremorgenic toxins
Stomach contents analysis Differentiate from strychnine or ethylene glycol toxicity** Treat: diazepam ± effective, activated charcoal
56
Toxins causing toxicity with tremorgenic toxins
Lolitrems A & B in perennial rye grass Paspalitrems in Bermuda & Dallis grass Fumitremorgens in ergot sclerotia
57
Chronic clinical signs of tremorgenic toxins
Onset 7-10 days - moderate morbidity, low mortality Muscle tremors, paralysis, nystagmus/anisocoria, hypersalavation, vomiting, ataxia, hypermetria, hyperesthesia
58
Diagnosing /treating tremorgenic toxins
Feed analysis, field assessment, ergot sclerotia in hay assessment Change feed/remove toxins Sedate animals as needed to protect from CNS signs
59
Endotoxins cause
Inflammatory reaction
60
Enterotoxins cause
Fluid and electrolyte loss

SS - Exam 1 (33 decks)

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