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Pathology > Neuro path: study guide (farina) > Flashcards

Neuro path: study guide (farina) Flashcards

1
Q

Function of oligodendrocytes

A

Form myelin in the CNS

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2
Q

Function of astrocytes

A

They form the BBB

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3
Q

Function of microglia

A
  • Phagocytic cells of the CNS
  • They have a small nuclei and little cytoplasm
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4
Q

What is central chromatolysis

A
  • Response of the nervous sytem to injury - neuronal change
  • Cells swollen with central clearing due to dispersio of Nissl substance
  • Nucleus is peripherally displace
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5
Q

What is neuronophagia

A

Phagocytes (microglia) gather around necrotic nucle and phagocytose it to remove debris

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6
Q

histologic characterisctics of neuronal degeneration

A
  • Empty, dilated axon sheaths
  • Gitter cells in digestive chambers
  • Vacuolization of axons
  • Spheroids
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7
Q

Spheroid

A
  • Focal axonal swellings filled wtih degenerative organelles
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8
Q

Type of necrosis typically seen in CNS, and characteristics of this type of necrosis

A
  • Liquifactive necrosis
  • Seen with ischemic injury to CNS like infarcts
  • Cells digested by liquefaction and all cell outlines are absent
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9
Q

Astrocytosis

A

Increase in number and size of astrocytes in response to injury

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10
Q

Gemistiocytic astrocytes

A
  • Plump, reactive astrocytes with eosinophilic (red) cytosplasm
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11
Q

Appearance of Alzheimers type II astrocytes

What disease process are these typically seen in

A
  • Swollen with large nuclei and chromatin clearing
  • Occurs with hyperammonemia
    • often due to hepatic encephalopathy
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12
Q

Hydroencephalus

A

Abnormal accumulation of fluid in crania cavity

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13
Q

Types of hydroencephalus

A
  • Internal: fluid in ventricles
  • External: fluid in arachnoid space
  • Communicating: fluid in ventricles and arachnoid space
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14
Q

Breed commonly affected by hydroencephalus

A

Brachycephalic breeds

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15
Q

Microencephaly

A

Abnormally small brain

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16
Q

Hydranencephaly

A
  • Near complete or complete absence of cerebral hemispheres, leaving fluid filled sacs formed by minges filled with CSF
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17
Q

Porencephaly

A
  • Cystic cavitation of the brain, usually involving cerebral white matter
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18
Q

Lissencephaly

A

lack of normal gyri and sulci on brain

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19
Q

anencephaly

A

absence of brain

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20
Q

Prosencephalic hypoplasia

A
  • absence of cerebral hemisphere but has brainstem
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21
Q

Cranium bifidum/spina bifida

A
  • defect in dorsal midline through which meninges and brain can extrude
  • Meningocele: herniation of meninges
  • Meningoencephalocele: herniation of meninges and brain
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22
Q

Most common brain malformation seen with BVD

A

cerebellar hypoplasia

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23
Q

What is the underlying cause of storage disease

A
  • Defects in lysosomal enzymes within the catabolism stage
24
Q

What happens to cells that accumulate substrate in lysosomal storage diseases?

A
  • Tissues that accumulate substrate first are those that are most active, they cannot clear material so their normal cellular functions get disrupted and the cell will eventually die
25
Q

How are storage diseases inherited?

When do they present with neuro signs?

A
  • Autosomal recessive
  • Present early in life with neuro signs
  • Progressive and fatal dsease
26
Q

How are the storage diseases named

A
  • Named according to class of molecule whose degeneration is defective
27
Q

What cells in the CNS are most sensitive to ischemia?

A
  • Neurons and oligodentocytes
  • Grey matter is more sensitive than white matter
28
Q

Causes of polioencephalomalacia?

Where are the lesions located?

A
  • Causes
    • high sulfur intake
    • deficiency of thiamine
    • disturbance of thiamine metabolism
  • Lesions
    • laminar softening of grey matter in cerebral cortex
29
Q

Cause of leukoencephalomalacia?

Where are the lesions located?

A
  • Cause
    • consumption of moldy corn for > 1 month
    • causes a mycotoxicosis due to fumonisin
  • Lesions
    • cerebral white matter necrosis
30
Q

Lesions of indirect salt poisoning?

What are the causes

A
  • Cause
    • high salt diet with restricted water access
    • occurs in swine
  • Lesions
    • cerebral edema
    • laminar cortical necrosis
    • eosinophilic meningoencephalitis
31
Q

Ways in which bacterial infections get into CNS

A
  • Heatongenous
  • Direct invasion
    • through the cribiform plate
    • through the middle ear
32
Q

In what species do we see listeriosis?

What is the causative agent?

A
  • Ruminants who eat a lot of silage
  • Listeria monocytogenes
33
Q

What are the characteristic lesions of listeriosis?

Where are they located?

A
  • Lesions
    • micro abscesses in the brainstem
  • Often in focus of microgliosis
34
Q

Pathogenesis of the encephalitis of listeriosis?

A
  • Bacteria spread up the motor and sensory branches of the trigeminal nerve
35
Q

What is the causative agent of thrombotic meningoencephalitis?

What species does it affect?

A
  • Histophilus somni
  • Affects cattle and sheep, especially young feedlot cattle
36
Q

Pathogenesis of development of CNS lesions of thrombotic meningoencephalitis?

What are the lesions?

A
  • Pathogenesis
    • Septicemia leads to cerebral vasculitis with hemorrhage, necrosis, and thrombosis
  • Gross lesions
    • multifocal hemorrhage and necrosis
  • Histologic lesions
    • vasculitis, thrombosis, infarction, neutrophilic meningoencephalitis
37
Q

General histologic features of viral infections

A
  • Non-suppurative meningoencephalitis
  • +/- myelitis
  • Perivascular cuffing
  • Gliosis: infiltration of glial cells
  • +/- viral inclusions
  • +/- neuronal degeneration/necrosis
38
Q

Principal reservoirs for rabies in the US

A
  • Skunks
  • Raccoons
  • Foxes
  • Bats
39
Q

What tissues is the rabies virus trophic for?

A
  • CNS
  • Salivary gland
40
Q

Pathogenesis of rabies from inoculation to spread to CNS

A
  • Virus inoculated into wound from bite - virus replicates in muscle cells near inoculation site - spreads to sensory paravertebral ganglia - virus travels along peripheral nerves to CNS
41
Q

What do lesions in rabies look like?

A
  • Non-suppurative encephalomyelitis
  • ganglioneuritis
  • parotid adenitis
  • amount of inflammation and neuronal degeration varies
  • Negri bodies (cytoplasmic inclusions) present most often in hippocampus in carnivores and Purkinje cells in herbivores
42
Q

What is the cause of pseudorabies

A

Porcine herpes virus 1

43
Q

Species affected by pseudorabies disease

A

can affect all common domestic species

44
Q

CS pseudorabies in pigs

A
  • Young
    • prostration
    • convlusions
    • twitching
    • high mortality rate
  • Sows
    • SMEDI
45
Q

CS of seudorabies in other species

A
  • Intense pruritis
  • fever
  • neuro signs (high mortality)
46
Q

CS of caprine arthritis encephalitis virus

A
  • Goat:
    • kids 2-4 months
    • Hind Limb ataxia
    • paresis
    • paralysis
    • death
  • Adults
    • mastitis
    • pneumonia
    • arthritis
47
Q

CS of Visna-Maedi virus

A
  • Sheep > 2 yrs old
  • Hind limb ataxia
  • lip trembling
  • Hind limb paresis
  • death due to secondary infection and starving
  • Adults
    • mastitis
    • pneumonia
    • arthritis
48
Q

Lesions associated with caprine arthritis encephalitis virus

A
  • Non suppurative leukoencephalomyelitis
  • demyelination
49
Q

Species typically affected by Cryptococcus neoformans

A
  • Cats
  • Dogs
  • Horses
50
Q

How do Visna-Maedi viruses get to the brain

A
  • Starts in nasal or sinus infection, enters through direct invasion through cribiform plate
51
Q

What are the histologic lesions of the cryptococcus

A
  • Thick, non-staining mucopolysaccharide capsule, makes it look like soap bubbles on tissue sections
52
Q

Infectious agent of equine protozoal myelopathy

A
  • Sarcocystic neurona
53
Q

Why are organisms not usually seen in most cases of EPM

A

Most animals have been treated for EPM before they were euthanized

54
Q

Cause of transmissible spongiform encephalopathies

A
  • Prions
  • Normal is PrPC and changed into abnormal form PrPSc
55
Q

How do animals typically acquire TSEs

A
  • Horizontal transmission
  • Due to consumption of infected feed material
56
Q

What are the lesions of TSE

A
  • Intracytoplasmic neuronal vacuolation
  • astrocytosis
57
Q

Difference between static and dynamic stenosis in wobblers

A
  • Dynamic
    • compression of spinal cord only when horse bends or extends neck
    • usually occurs in young animals
    • C3-C4 and C4-C5 usually affected
  • Static
    • Occurs regardless of position of neck
    • usually older animals
    • C5-C6 and C6-C7 usually affected

Pathology (6 decks)

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