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425 - sys path > Neuro 4 > Flashcards

Neuro 4 Flashcards

1
Q

What are the two big small ruminant Lentiviruses that we need to know?

A

Caprine arthritis encephalitis virus (CAEV)
Maedni Visna (MV)

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2
Q

who does caprine arthritis encephalitis virus affect?

A

goats

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3
Q

who does Maedni visna virus affect? what is the other name for the disease?

A

Sheep
ovine progressive pleuropneumonia

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4
Q

What are the 4 body systems that small ruminant lentiviruses target?

A

CNS, lung, joints, mammary gland

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5
Q

what do small ruminant Lentiviruses do to the CNS?

A

nonsuppurative leukoencephalomyelitis

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6
Q

Lentiviruses form _____ in joints.

A

Hygromas

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7
Q

what are two ddx’s for a hygroma?

A

Brucella, Lentivirus

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8
Q

true or false: Lentivirus infection is a lifelong virus

A

true

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9
Q

what is this?

A

hygroma

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10
Q

Small ruminant lentiviruses:
1) how are they transmitted?
2) infect what cell type
3) what is the important signalment for CAEV that we need to know?
4) what type of tissue does it impact in CNS?

A

1) colostrum/milk > resp droplets
2) monocytes/macrophages
3) goat kids <4mo old –> neuro disease ± pneumonia
4) white matter (demyelinating disease)

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11
Q

who is affected by rabies?

A

all mammals!

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12
Q

what is the pathogenesis of rabies?

A

1) bitten/scratched by rabid animal
2) local replication in muscle or peripheral nerve
3) binds acetylcholine receptors at neuromuscular junction
4) fast retrograde axonal transport to CNS
5) antergrade axonal transport to salivary gland

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13
Q

what re the 3 phases of rabies? what are the two forms and what do they mean?

A

phases: prodromal, excitatory, paralytic
forms:
- furious form –> excitatory predominates
- dumb form –> paralytic predominates

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14
Q

what are the important gross and histo findings of rabies?

A

gross: none
histo: Negri bodies, can be minimal!

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15
Q

Prion diseases are also known as ______.

A

Transmissible Spongiform Encephalopathies (TSE)

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16
Q

what causes prion disease?

A

prions (infectious proteins)
abnormal folding, don’t have DNA/genome

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17
Q

1) The normal version of prion proteins, ____, is coded from a highly conserved gene and is found ______.
2) the abnormal version, _____, is _____ resistant to things that would normally degrade DNA and protein.

A

1) PrPc, in most living things
2) PrPSc, highly

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18
Q

Prions cause _______ disease.

A

neurodegenerative

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19
Q

PrPSc has a species barrier. what does that mean?

A

PrPSc is slightly different in each species and doesn’t easily transmit between different species

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20
Q

what are the two ways of acquiring PrPSc?

A

Acquired and spontaneous mutation

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21
Q

what are the 3 acquired prion diseases that we need to know and how are they transmitted?

A

chronic wasting disease (CWD) - horizontal transmission (saliva, blood, urine, etc)
bovine spongiform encephalopathy (BSE) - ingestion
Scrapie - ingestion and possible vertical transmission

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22
Q

Prion diseases:
1) it can take ____ for enough atypical protein to accumulate to cause clinical disease.
2) is there an immune response to prion diseases? why/why not/
3) eventually ____, C/S variable but ____

A

1) years
2) no. body doesn’t recognize protein as foreign
3) fatal, progressive

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23
Q

what are the gross and histo findings of prion diseaseS?

A

gross: none
histo: no inflammation, vacuolation of neutrons and neuropil

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24
Q

What are the 4 causes of polioencephalomalacia?

A
  1. thiamine deficiency (Vit B1)
  2. sulfur toxicity
  3. lead toxicity
  4. salt toxicity/water deprivation
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25
Q

in adult ruminants, thiamine is produced by _____ in _____.

A

bacteria, rumen

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26
Q

what is the important way that thiamine deficiency happens in ruminants?

A

disruption of rumen flora production of thiamine (ruminant acidosis, grain overload, for ex)

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27
Q

true or false: for polioencephalomalacia, the gross + histo lesions are the same for carnivores and herbivores.

A

false. they are different!

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28
Q

what are the gross lesions of polioencephalomalacia in herbivores?

A

targets deep gray matter of the cerebral cortex
bilaterally symmetric
yellow discolouration (can be autofluorescence)

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29
Q

what most likely caused this lesion? ruminant brain

A

polioencephalomalacia

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30
Q

what is the important histo lesion of polioencephalomalacia in herbivores?

A

laminar cortical necrosis

31
Q

what are the gross lesions of polioencephalomalacia in carnivores?

A

bilaterally symmetric
periventricular grey matter, esp in brain stem, caudal colliculi

32
Q

what most likely caused this lesion? carnivore brain

A

polioencephalomalacia

33
Q

what are the 2 ways that salt toxicity/water deprivation in pigs and poultry occurs?

A
  1. direct - over consumption of salt
  2. indirect - water deprivation followed by sudden unlimited access to water
34
Q

how does salt toxicity/water deprivation cause polioencephalomalacia in pigs and poultry? like give me the pathogenesis

A
  1. hypernatremia
  2. fluid moves from brain/CSF to blood
  3. Na, K, Cl move into brain
  4. animals consume water
  5. water moves rapidly into brain = edema
35
Q

what is the important histo feature that salt tox/water deprivation polioencephalomalacia in pigs causes?

A

eosinophilic infiltrate within meninges and perivascular spaces

36
Q

what is the cause of equine leukoencephalomalacia?

A

ingestion of mouldy corn

37
Q

what is the etiology of equine leukoencephalomalacia?

A

Fusarium moniliforme –> forms toxin fumonisin B1

38
Q

what are the gross findings of a horse with equine leukoencephalomalacia?

A

edema
bilateral, but NOT SYMMETRIC!!! malacia and liquefaction of the subcortical white matter

39
Q

horse brain. what is the disease?

A

equine leukoencephalomalacia

40
Q

Nigropallidal encephalomalacia: how does it happen in horses?

A

horses that graze on Centaurea spp. of plants (yellow star thistle and Russian knapweed)

41
Q

what is the important clinical sign of nigropallidal encephalomalacia in horses?

A

persistent chewing movement without feed in mouth

42
Q

what are the gross findings of nigropallidal encephalomalacia? where are lesions targeted?

A

bilaterally symmetric, well-demarcated areas of yellow discolouration and malacia
globus pallidus and substantia negra

43
Q

what is the lesion?

A

nigropallidal encephalomalacia

44
Q

Domoic acid toxicity:
1) who gets it?
2) how do they get it?
3) gross lesion?
4) clinical sign?

A

1) birds, marine mammals
2) marine algae (red tides)
3) hippocampal atrophy
4) seizures

45
Q

brain of a bird (hippocampus). what caused this

A

domoic acid toxicity

46
Q

what are the 3 types of canine idiopathic encephalitides?

A
  1. granulomatous meningoencephalitis (GME)
  2. Necrotizing meningoencephalitis (NME)
  3. necrotizing leukoencephalitis (NLE)
47
Q

what is the common signalment for granulomatous meningoencephalitis?

A

young-middle aged small breed dogs

48
Q

what is the lesion we have to know for granulomatous meningoencephalitis?

A

distinct macrophage perivascular cuffs restricted to the white matter

49
Q

what is the common signalment for necrotizing meningoencephalitis?

A

small breed dogs (ex. pug, Shih Tzu, Maltese)

50
Q

what tissue type is mainly affected with necrotizing meningoencephalitis?

A

grey matter

51
Q

what is the common signalment for necrotizing leukoencephalitis

A

Yorkshire terriers

52
Q

what is the lesion we have to know for necrotizing leukoencephalitis?

A

caveatting non-suppurative areas of necrosis in white matter of cerebrum

53
Q

CNS tumors are more common in ____ than other species, and ______ and ______ are predisposed

A

dogs, golden retrievers, brachycephalic breeds

54
Q

what is the most common tumor of the CNS?

A

meningioma

55
Q

what species are meningiomas most common in?

56
Q

what lesion is this? this is a cat brain

A

meningioma

57
Q

?cat brain. lesion

A

meningioma

58
Q

Ependymomas are common in what signalment?

A

brachycephalic breeds

59
Q

where are ependymomas most common in? like tissue area

A

lateral ventricles

60
Q

pug brain. what this?

A

ependymoma

61
Q

Ependymomas can cause ____ anterior to the tumor.

A

hydrocephalus

62
Q

choroid plexus tumors are most common in what location?

A

4th ventricle

63
Q

what is the common signalment for choroid plexus tumors?

A

golden retrievers

64
Q

what is the gross appearance of choroid plexus tumors?

A

granular to papillary growth

65
Q

brain of golden retriever. what this?

A

Choroid plexus tumor

66
Q

what are the 4 types of glioma? how are they named?

A
  1. oligodendroglioma
  2. astrocytoma
  3. Gliomatosis cerebri
  4. mixed

named for cell of origin (except gliomatosis cerebri, it’s from microglial cells but the origin is controversial)

67
Q

gliomas are most common in _____, especially what breeds?

A

dogs
Boston, Boxer, Bulldog

68
Q

Boston terrier brain. what?

A

glioma of some type

69
Q

true or false: all gliomas are considered benign

A

FALSE! all are considered malignant

70
Q

What is the other name for a cholesteatoma?

A

cholesterol granuloma

71
Q

cholesteatomas are a common finding in ______

A

aged horses

72
Q

what ist eh gross appearance of choesteatomas?

A

yellow brown firm nodular mass within ventricles that can be mineralized

73
Q

25 year old horse brain. what this?

A

cholesteatoma

74
Q

true or false. cholesteatomas cause a ruckus in the brain

A

false. they are predominantly asymptomatic

425 - sys path (38 decks)

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