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Sys Path > Nervous System > Flashcards

Nervous System Flashcards

1
Q

Grey matter

A

neurons – horns of the spinal cord, cerebellar/cerebral cortex

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2
Q

White matter

A

myelinated axons – medullary center of brain, outer cortex of spinal cord

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3
Q

What is the function of oligodendrocytes?

A

Form myelin the wraps around axons (CNS)~ similar to Schwann cells in PNS

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4
Q

What is the function of Astrocytes?

A

cell processes form BBB and repair CNS after injury

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5
Q

What is the function of Microglia?

A

Phagocytic cells “fixed macrophages of CNS”

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6
Q

What is central chromatolysis?

A

Response of nervous system to injury involving degenerative change & swelling with dispersal of Nissl substances

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7
Q

What is neuronophagia?

A

Occurs when microglia surround degenerate or necrotic neurons and phagocytose it to remove debris

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8
Q

What are the histologic characteristics of axonal (Wallerian) degeneration?

A

i. Axon degeneration (spheroid appearance~ swollen/eosinophilic)
ii. Gitter cells remove axon & myelin debris (microglia with foamy cytoplasm)
iii. Empty dilated axon sheaths  cant regenerate in CNS

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9
Q

What is a spheroid?

A

Focal axonal swellings filled with degenerate organelles

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10
Q

What is astrocytosis?

A

increase size & number of astrocytes in response to injury

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11
Q

What are gemistocytic astrocytes?

A

Plump reactive astrocytes with eosinophilic cytoplasm~ look like necrotic neurons but have healthy nucleus

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12
Q

What is the appearance of Alzheimer’s type II astrocytes, and what disease process are these cells typically seen in?

A

appear “reactive” found around neurons, enlarged with vesicular nuclei. Found with hepatic encephalopathy

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13
Q

What are the different types of hydrocephalus?

In which breeds of dog is hydrocephalus most common?

A

Internal (fluid in ventricles- most common), External (fluid in arachnoid space) & communicating (fluid in ventricles & arachnoid space)

  • Brachycephalic dogs
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14
Q

Hydranencephaly

A

near complete/ complete absence of cerebral hemispheres~ have CSF fluid filled sacs formed by meninges. Often associated with arbovirus or pestivirus

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15
Q

Porencephaly

A

cystic cavitation of brain (involves white mater)~ occur later in development

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16
Q

Lissencephaly

A

brain lacking normal gyri & sulci, this is not normal for domestic mammals (everything that is non-mammal normally lissencephalic)

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17
Q

Prosencephalic hypoplasia

A

cerebral aplasia; absence of cerebral hemispheres with preservation of some portion of the brainstem

18
Q

Cranium bifidum/spina bifida

A

defect which brain/ spinal cord & meninges can protrude~ almost always dorsal midline

19
Q

What is the underlying cause of storage diseases?

A

Defective catabolism (often result of a defect in lysosomal enzyme)

20
Q

How are storage diseases named

A

Named according to the substance that has defective degradation

21
Q

How are storage diseases inherited, and when do they typically present with neurologic signs?

A

Usually autosomal recessive condition & present with neurologic signs early in life.

22
Q

Which cells in the CNS are most sensitive to ischemia?

A

Neurons & oligodendroglia; grey matter is more sensitive than white d/t to its higher O2 dependence.

23
Q

polioencephalomalacia causes

A

Necrosis of grey matter, causes often unknown~ however thiamine deficiency / disturbance high sulfur intake & water deprivation may be implicated

24
Q

Distribution: Asymmetric vs symmetric lesions

A

Asymmetric: infectious
Symmetric: think systemic- toxin, nutritional or metabolic

25
Q

What causes leukoencephalomalacia?

A

moldy corn consumption (fumonisin toxin)

26
Q

What causes indirect salt poisoning? What are the associated lesions?

A

Ingestion of high salt diet + restricted water intake

- Cerebral edema, laminar cortical necrosis, nonsuppurative and eosinophilic meningoencephalitis.

27
Q

What are the ways in which bacterial infections commonly get to the CNS?

A

Septicemia (young animal), septic emboli (endocarditis) & abscess (hematogenous spread or direct invasion via cribriform plate/ middle ear)

28
Q

In what species do we most often see listeriosis or “circling disease”?

a. What is the causative agent of listeriosis?
b. What are the characteristic lesions, and where are the lesions typically located?

A

ruminants

Listeria monocytogenes

Microabscesses, sometimes within foci of microgliosis. Typically located in brainstem

29
Q

What is the causative agent of thrombotic meningoencephalitis (ITME)?

A

Histophilus somni

30
Q

What is ITME pathogenesis in development of CNS lesions, and what are the lesions?

A

Septicemia then cerebral vasculitis with hemorrhage, necrosis and thrombosis. You’ll see vasculitis, thrombosis, infarction, neutrophilic meningoencephalitis and it can form abscesses

31
Q

What are the general histologic features of viral infections?

A

Non-suppurative meningoencephalitis, perivascular cuffing, gliosis +/- viral inclusions & neuronal degeneration

32
Q

What are the principal reservoirs for rabies in the US?

A

Skunks, foxes, bats & raccoons

33
Q

What is the pathogenesis of rabies viral infection from inoculation to spread to the CNS?

A

Virus inoculated in wound (bite)–>virus replicates in muscle cells (near inoculation site) & spreads to sensory ganglia, then travels along peripheral nerves to CNS

34
Q

Pseudorabies clinical signs

A

i. Spp other than pigs: pruritis, high mortality, fever & neurologic fatal
ii. Pig: mild fever, no pruritis, but may see convulsion and high mortality rate in piglets. Soes- abortion, stillborn & mummified fetus

35
Q

What are the clinical signs of caprine arthritis-encephalitis virus and visna-maedi virus?

A

Hind limb ataxia, paresis, paralysis, death (CAE causes arthrtitis in adults; VM causes pneumonia)

36
Q

In what age animals is neurologic disease typically observed in CAE & VM?

A

i. CAE: kids 2-4 mo.

ii. Visna-maedi: sheep > 2 yo

37
Q

What are the lesions associated with CAE & VM?

A

i. CAE: non-suppurative leukoencephalomyelitis, demyelination
ii. Visna-maedi: nonsupprative meningoencephalitis (affect white matter) & demyelination

38
Q

Cryptococcus neoformans species, how it gets in brain & histologic lesions?

A
  • spp: cat, horse & dog
  • Starts as nasal or sinus infection–>enters brain (direct extension through cribriform plate); can also spread to brain hematogenous from pulmonary infection
  • Non-staining mucopolysaccharide capsule (soap bubble appearance).
39
Q

Cause of equine protozoal myelitis?

A

Sarcocystis neurona

40
Q

What are the lesions of TSEs?

A

Intracytoplasmic neuronal vacuolation & astrocytosis

Sys Path (8 decks)

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