Toxins Flashcards

1
Q

What is the active toxic component of blue green algae toxicity?

A

microcystin-LR

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2
Q

what is the active toxic component of cycad toxicity

A

methylazoxymethanol

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3
Q

What category of hepatotoxin is trematoxin (poison peach)?

A

glycoside

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4
Q

What is the active toxic component of jasmine (non-diurnum Cestrum)?

A

atractyloside

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5
Q

What are some examples of plants with excessive amounts of PA’s?

A

Crotalaria, Trichodesma, Senecio

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6
Q

What mineral toxin causes both hepatic and renal toxicity?

A

copper

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7
Q

What is a good differential for blue green algae toxicity?

A

aflatoxin

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8
Q

Histo features of acetaminophen toxicity? Clin path findings?

A

sinusoidal lining cell necrosis and centrilobular to submassive hepatic necrosis; ALT, AST elevations. Acute, nonregenerative anemia with Heinz body formation and eccentrocytes, severe methemoglobinemia.

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9
Q

What common anti-neoplastic causes cardiotoxicity in animals and humans?

A

doxorubicin

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10
Q

The neurotoxic components of blue green algae include?

A

anatoxin, saxitoxin

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11
Q

Neurotoxic component of chocolate

A

theobromine

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12
Q

All of the following are excitatory neurotoxins except: A. Strychnine B. Pyrethrin C. Lead D. Ivermectin

A

D. Ivermectin. Along with ethylene, ivermectin is one of the few CNS depressant neurotoxins of animals. Bromethalin can have both excitatory and depressant presentations.

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13
Q

The neurotoxic cause of leukoencephalomalacia in horses is?

A

Fumonisin B1 produced by Fusarium spp.

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14
Q

The toxic component of locoweed (Astragalus spp.) is?

A

Swainsonine

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15
Q

This plant causes nigropalladial malacia in horses?

A

Yellow star thistle (Centaurea solsitialis); toxic agent is repin

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16
Q

What is the pathogenesis of Cestrum diurnum toxicity

A

vitamin D analog

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17
Q

What is the active toxic component of red maple leaf in horses?

A

gallotannins

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18
Q

What are 3 toxic differentials for tubular necrosis in a dog?

A

ethylene glycol, NSAIDS, grapes/raisins

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19
Q

What is a toxic differential for renal tubular necrosis in chickens?

A

monensin

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20
Q

What are two toxic differentials for renal tubular necrosis in pigs?

A

pigweed (Amaranthus sp.) and ochratoxin

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21
Q

What is a toxic differential for renal tubular necrosis in chickens?

A

monensin

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22
Q

What are 3 toxic differentials for tubular necrosis in a dog?

A

ethylene glycol, NSAIDS, grapes/raisins

23
Q

What is the active toxic component of red maple leaf in horses?

A

gallotannins

24
Q

What is the pathogenesis of Cestrum diurnum toxicity

A

vitamin D analog

25
Q

Swainsonine causes pathology via:

A

inhibition of lysosomal alpha-mannosidase leading to alpha-mannosidosis

26
Q

The toxic component of locoweed is

A

swainsonine

27
Q

Phalaris, or reed canary grass, poisoning results in two acute neurological clinical presentations. What are they?

A

Sudden death from cardiotoxic compounds in sheep and horses and polioencephalomalacia-like syndrome in sheep

28
Q

Histologically, Phalaris poisoning is characterized by:

A

storage of granular pigment in the neurons of the brainstem, spinal cord and dorsal root ganglia

29
Q

Clinical signs of cyanide toxicity include:

A

Peracute: bright red blood due to oxygen saturation, dyspnea, drooling, trembling, recumbency, seizures. Acute (> 1 hr): vomiting (especially in pigs), nystagmus, cyanosis. Dark blood later in the clinical course is due to anoxia.

30
Q

The mechanism of cyanide toxicity is through inhibition of:

A

intracellular respiratory enzymes

31
Q

Necropsy signs of cyanide toxicity include:

A

cardiorespiratory edema and epicardial/lung hemorrhages

32
Q

Examples of cyanogenetic plants are:

A

Sorghums, star grasses (Cyanodon spp), cherry and linseed

33
Q

Cyanide is converted to thiocyanate in the rumen and can cause this gross lesion:

A

goiter

34
Q

Nitrite toxicity is the result of the conversion of hemoglobin to what compound that causes a “dark chocolate” color in the blood?

A

methemoglobin

35
Q

Carbon monoxide poisoning is characterized by what gross change?

A

Bright pink to red tissues and diffuse congestion of all organs, especially the brain d/t vessel dilation

36
Q

Tissue from a horse. This lesion is most likely the result of:

A

yellow star thistle (Centaurea solstitialis) or Russian knapweed (Centaurea repens) toxicity.

37
Q

What is the toxic compound of Centaurea sp?

A

repen

38
Q

How does repin cause nigropallidal encephalomalacia?

A

glutathione depletion –>oxidative damage –> mitochondrial dysfunction –>neuronal cell death

39
Q

Salt poisoning in pigs is the result of:

A. excessive consumption of high salinity drinking water

B. excessive salt intake with reduced access to drinking water

C. excessive consumption of salt with adequate access to drinking water

A

B. excessive salt intake with reduced access to drinking water. This is considered “indirect salt poisoning” and imparts the characteristic neurologic disease.

40
Q

The pathognomonic lesions of salt toxicity in pigs are (2):

A

laminar cortical necrosis and cerebral eosinophilia of the Virchow-Robbins spaces and meninges

41
Q

Leukoencephalomalacia in horses is the result of toxicity from what?

A

Fumonisin B1, a product of Fusarium verticilloides and F. proliferatum which are molds that grow on corn (“moldy corn toxicity”)

42
Q

Fumonisin B1 toxicity may result in all of the following lesions in horses except:

A. hepatic necrosis

B. necrosis of the white matter

C. necrosis of the gray matter

D. icterus

A

C. necrosis of the gray matter is found in PEM, not leukoencephalomalacia due to moldy corn toxicity in horses. Some horses can have hepatic lesions leading to hepatic encephalopathy and icterus

43
Q

The release of spinal motor neurons from the inhibitory influence of “Renshaw” cells (inhibitory neurons) leads to the extensor spasms and hyperesthesia that characterize what two forms of poisoning?

A

Tetanus and Strychnine

44
Q

Strychnine causes spasms through the (presynaptic/postsynaptic) blockade of the (inhibitory/excitatory) neurotransmitter glycine.

A

post-synaptic; inhibitory. It blocks the receptors. Tetanus is pre-synaptic but also blocks glycine.

45
Q

Mercury toxicity causes what histologic lesions:

A. acute tubular renal injury, degeneration of the Purkinje cells of the heart, cerebellar granular layer degeneration, acute neuronal degeneration

B. acid-fast inclusions in the renal tubular epithelium, polioencephalomalacia

A

A. The lesions listed in B are for lead toxicity.

46
Q

The toxic components of Cycad toxicity are:

A. Cycasin, macrozamin and methylazoxymethanol

B. Swainsonine

C. Repin

D. Gallotannins

A

A. The first two are inactive, the last is the active component.

47
Q

Tremorgens are the toxin group responsible for the disease known as :

A. Hairy shaker disease

B. Perrenial rye grass staggers

C. Fog fever

D. Mycotoxic leukoencephalomalacia

A

B. Perrenial rye grass staggers is caused by lolitrems, a group of tremorgen toxins produced by the fungus Neotyphodium lolii. The grass itself is called Lolium perrene. A. is Border Disease virus. C. is atypical interstitial pneumonia (now known as acute bovine pulmonary edema and emphysema or ABPEE) caused by L-tryptophan. D. is caused by another fungus, Fusarium sp. which produces fumonisin B1 and occurs in horses.

48
Q

Torpedo-type Purkinje cells in the cerebellum may sometimes be seen in what toxicity?

A. Lead

B. Mercury

C. Swainsonine

D. Lolitrem (Perrenial Rye Grass Staggers)

A

D. this is the only histologic lesion, and it is not consistently found.

49
Q

Moderate poisoning of inorganic arsenicals produces lesions based on what common finding?

A

vascular injury = hemorrhages in multiple organs, including the brain.

50
Q

Secondary copper deficiency in ruminants is primarily through:

A. Antagonism by zinc

B. Antagonism by sulfur

C. Antagonism by molybdenum

A

C. molybdenum is the primary copper antagonist in the ruminant, where in the rumen molybdenum complexes with sulfur and copper to form insoluble molecules.

51
Q

Swayback is another name for deficiency of what?

A. molybdenum

B. zinc

C. Vitamin A

D. copper

A

D. copper deficiency, swayback and enzootic ataxia are all terms for the same deficiency. They refer to a neonatal form and occur in sheep, goats and pigs. Swayback refers to the congenital form. Enzootic ataxia specifically refers to a delayed onset of clinical signs where animals are clinically normal at birth and then develop signs within one week of age.

52
Q

What type of toxicity does oak poisoning cause?

A

renal toxicity; acute tubular necrosis

53
Q

Give 3 cardiotoxins of horses. What are other differentials of an equine heart with endocardial hemorrhages besides toxicity?

A

Oleander leaves, taxus (i.e. yew plant), monensin, ouibain (African plants). All change concentration of Na in cells, accumulate Na in cell, Ca2+ influx, actin and myosin filament contraction and mitochondrial disruption -> dysrhythmia. Another differential would be purpura hemorrhagica: usually secondary to bacterial infection –> deposition of Ag-Ab complexes in vascular walls –> activation of complement –> leukocytoclastic vasculitis –> multifocal hemorrhages of mostly skin but other organs too –> severe dependent edema (limbs). Others would be endotheliotropic viruses like equine arteritis virus, Equine herpes virus-1, Hendra or African horse sickness (Orbivirus)

54
Q
A