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Pathology I > Lecture 5: Toxic and Nutritional Neuropathies > Flashcards

Lecture 5: Toxic and Nutritional Neuropathies Flashcards

1
Q

What does malacia mean

A

Necrosis

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2
Q

What does polioencephalomalacia mean

A

Necrosis of the gray matter within the brain

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3
Q

What does poliomyelomalacia

A

Necrosis of the gray matter of the spinal cord

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4
Q

What is leukoencephalomalacia

A

Necrosis of the white matter of the brain

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5
Q

What is leukomyelomalacia

A

Necrosis of the white matter of the spinal cord

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6
Q

Describe what you are seeing and what caused this

A

loss of vacuolation of tissue with minimal inflammation

Macrophages (gitter cells) influx to clean up necrotic neuroparenchyma

Malacia

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7
Q

What diseases are associated with Multifocal, bilaterally symmetric malacia

A
  1. Yellow star thistle
  2. Clostridium perfringes type D
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8
Q

What diseases are associated with laminar malacia

A
  1. Poliencephalomalacia
  2. Leukoencephalomalacia
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9
Q

What species typically gets nigropallidal encephalomalacia

A

Horses

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10
Q

What causes nigropallidal encephalomalacia

A

Yellow star thistle

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11
Q

What is the pathogenesis for nigropallidal encephalomalacia

A
  1. Prolonged ingestion of yellow star thistle
  2. Repin neurotoxin
  3. Oxidative damage
  4. Neuronal cell death
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12
Q

What are the gross findings associated with nigropallidal encephalomalacia

A

Bilaterally symmetric malacia of globus pallidus and substantia nigra
White and gray matter affected

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13
Q

Horse brain- what wrong and cause

A

Nigropallidal encephalomalacia caused by yellow star thistle toxicosis

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14
Q

What species typically get C. Perfringes type D epsilon toxicosis

A

Small ruminants

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15
Q

What is pathogensis of C. Perfringens type D Epislon toxicosis

A
  1. Excess grains
  2. Promotes C. Perfringes type D overgrowth in the intestine
  3. Epislon toxin permeates into circulation
  4. Endothelial damage and increased vascular permeability
  5. Brain edema
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16
Q

Histology from sheep brain who recently ate an entire bag of grain. What does histo show and what is cause

A

histo: brain edema
C. Perfringes Type D epsilon toxicosis

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17
Q

What are the gross findings associated with C. Perfringes type D epsilon toxicosis

A

Bilaterally symmetric malacia of basal ganglia and brainstem
White and gray matter affected

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18
Q

Goat brain- what wrong and what cause

A

Encephalomalacia of basal ganglia caused by C. Perfringes type D epsilon toxicosis

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19
Q

What are some causes of polioencephalomalacia

A

Thiamine deficiency, salt toxicity, sulfur toxicity, lead toxicity, severe hypoglycemia, anoxia/hypoxia

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20
Q

How do areas with polioencephalomalacia appear

A

Gray matter is yellow-tan glistening layer that fluoresces under UV light

Cerebral edema which presents as flattening of gyri

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21
Q

What does polioencephalomalacia histology look like

A

Necrosis of cortical neurons

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22
Q

What happening in histo and what wrong

A

Cortical neuron necrosis
Cause: polioencephalomalacia

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23
Q

What wrong

A

polioencephalomalacia- flattening of gyri

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24
Q

How does thiamine deficiency cause polioencephalomalacia

A

Thiamine is produced by bacteria in the rumen and decreased when you ingest thiaminases like bracken fern or thiamine analogs

Decreased production by rumen microbes typically associated with increased grain intake

25
Q

What species is thiamine deficiency most common in

A

Ruminants- cattle, goats, sheep

26
Q

How does sulfur toxicosis cause polioencephalomalacia

A
  1. Excess sulfur in food or water
  2. Rumen microbes produce too much hydrogen sulfide which is absorbed into circulation
  3. Interferes with energy production
  4. Neurons need a lot of energy and lack of leads to cortical neuronal necrosis
27
Q

How does lead toxicity lead to polioencephalomalacia

A
  1. Lead enters circulation
  2. Mimicking Ca2+ it is able to cross BBB and enter neurons
  3. Oxidative stress
  4. Neuronal necrosis
28
Q

What species is typically affected by salt toxicity

A

Swine

29
Q

How does salt toxicity lead to polioencephalomalacia

A
  1. Decrease water
  2. Dehydration
  3. Na+ retention
  4. Accumulation Na+ in CSF
  5. Rapid water intake
  6. Rapid water influx into brain- edema—> cortical necrosis (water follows salt)
30
Q

What histological presentation is classic with salt toxicity in pigs

A

Eosinophilic inflammation

31
Q

Owner notices water troughs for pigs have been frozen over for days, he breaks it open and suddenly a lot of bigs die. The following histo was taken from the brain- what does it show and what caused this

A

histo: eosinophilic inflammation
Cause: salt toxicity leading to polioencephalomalacia

32
Q

How does hypoglycemia cause polioencephalomalacia

A

Brain needs high levels of glucose, so when low glucose—> lack ATP production—> cell death

33
Q

What are some causes of severe hypoglycemia

A
  1. Malnutrition/ anorexia
  2. Xylitol toxicity
  3. Excess insulin
  4. Juvenile hypoglycemia
34
Q

Moldy corn ingestion causes ___ in ___

A

Leukoencephalomalacia in horses

35
Q

What is pathogenesis of moldy corn ingestion causing leukoencephalomalacia in horses

A
  1. Prolonged ingestion of moldy corn with fumonosin spp
  2. Produces fumoisin B1
  3. Inhibits normal lipid synthesis in the brain leading to accumulation of sphingosine (toxic to white matter)
  4. Leukoencephalomalacia
36
Q

Horse ate lots of corn- then died, what happened

A

Moldy corn ingestion causing leukoencephalomalacia

37
Q

How are lysosomal storage neuropathies induced

A

Ingested plant toxins that inhibit lysosomal enzymes

38
Q

What does induced lysosomal storage neuropathies lead to

A

Abnormal accumulation of materials within neurons which disrupts their function

39
Q

Describe histo and what wrong

A

Abnormal neuron with vacuolated cytoplasm
Cause: lysosomal storage neuropathies

40
Q

What is an example of a disease that causes induced lysosomal storage neuropathy in horses

A

Locoweed (swainsonine) toxicosis

41
Q

How does locoweed toxicosis cause lysosomal storage neuropathy

A

Prolonged ingestion of swainsonine inhibits lysosomal enzymes

42
Q

Copper deficiency is common in what species

A

Young, small ruminants

43
Q

Vitamin E deficiencies are common in what species

A

Horses

44
Q

What is the purpose of vitamin E and copper and what does deficiency affect brain

A

Protect from oxidative stress, without increase oxidative stress-> neuronal cell death

45
Q

What does neonatal copper deficiency cause

A

Progressive central neurological signs with ascending hind limb paralysis

46
Q

What is the most common cause of neonatal copper deficiency

A

Secondary- reduced intestinal absorption due to other GI pathology or availability due to ingestion of copper antagonists

47
Q

What are some copper antagonists

A

Molybdenum, sulfate, iron, calcium

48
Q

Goat presents with ascending hindlimb paralysis. What nutritional deficiency can cause this

A

copper deficiency

49
Q

___is the primary source of vitamin E in equine diets

A

Green gas’s

50
Q

What two diseases can vitamin E deficiency cause in horses

A
  1. Equine degenerative myeloencephalopathy
  2. Equine motor neuron disease
51
Q

Vitamin E deficiencies inn horses can cause lesions in ___ and ___

A

Brain and spinal cord

52
Q

What is one of the top causes of spinal ataxia in young horses

A

Equine degenerative myeloencephalopathy due to vitamin E deficiency

53
Q

What horses get EDM

A

Young horses 6-24 months

54
Q

What breeds might have genetic disposition to EDM

A

Morgans, appaloosas, Lusitanos

55
Q

How do horses with EDM present

A

Symmetrical ataxia

56
Q

T or F: EDM horses have gross CNS lesions

A

False

57
Q

Who is affected by equine motor neuron disease

A

Adult horse >2yrs because requires prolonged deficiency

58
Q

What happens in equine motor neuron disease

A

Lower motor neurons targeted which are nerves that innervate muscles—> denervation atrophy

59
Q

What muscles are most commonly affected by equine motor neuron disease

A

Triceps brachii and vastus lateralis

Pathology I (23 decks)

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