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Pathology > Spr 16- Nervous Pathology- Farina > Flashcards

Spr 16- Nervous Pathology- Farina Flashcards

1
Q

Oligodendrocyte function

A

A glial cell that forms myelin around axons in CNS

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2
Q

Astrocyte function

A

Cell processes form the blood brain barrier

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3
Q

Microglia function

A

Phagocytic cells

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4
Q

Gitter cells

A

derived from microglia - after they have phagocytosed infectious material

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5
Q

What is central chromatolysis

A

Degenerative change, swelling of neurons with central clearing from Nissl substance dispersion, peripheral displacement of the nucleus

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6
Q

What is neuronophagia

A

In necrosis (eosinophilic cytoplasm), microglia gather around a necrotic neuron and phagocytose to remove debris

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7
Q

Histo characteristics of axonal degeneration

A

Wallerian degeneration - degeneration of the axon segment distal to the damage - dilation, empty, gitter cells in a digestion chamber - caterpillar cross section

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8
Q

What is a spheroid

A

focal axon swellings filled degenerative organelles

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9
Q

What kind of necrosis is typical in CNS, describe

A

Liquefactive - ischemic injury, cell outlines are absent and grossly looks like jelly

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10
Q

What is astrocytosis

A

Increase in size and number of astrocytes in respnse to injury because they are responsible for repair

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11
Q

What are gemistocytic cells

A

Astrocytes that are plump, reactive and filled with eosinophilic cytoplasm (bigger cell, bigger nucleus)

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12
Q

What do Alzheimer II cells look like

A

Swollen astrocytes with large nuclei with clearing around the nucleus - tend to flank neurons

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13
Q

What disease process are Alz II cells seen in

A

hyperammonemia

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14
Q

What is hydrocephalus

A

Accumulation of fluid in the cranial cavity

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15
Q

Internal hydrocephauls

A

Excess fluid in ventricles

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16
Q

External hydrocephalus

A

Excess fluid in arachnoid space

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17
Q

Communicating hydrocephalus

A

Fluid in both ventricles and arachnoid

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18
Q

Breeds predisposed to hydrocephalus

A

Brachycephalic, chihuahuas

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19
Q

Microencephaly

A

Small brain- cerebrum

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20
Q

Hydranencephaly

A

Little or no cerebral hemisphere - leaves fluid filled sacs (meninges filled with CSF)

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21
Q

Porencephaly

A

Cystic cavitation (from in utero infarcts) involving cerebral white matter

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22
Q

Lissencephaly

A

Absence of gyri and sulci (rodents, rabbits, some primates, non mammals, lhasa apsos)

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23
Q

Prosencephalic hypoplasia

A

No cerebral hemispheres but brainstem preserved - stems from dysraphia

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24
Q

Cranium bifidum

A

dysraphia defect in dorsal midline where meninges (+/- brain) can herniate

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25
Q

Spina bifida

A

Dysraphia defect in vertebral arch(es) leading to herniation of meninges +/- spinal cord (missing dorsal lamina that covers cord)

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26
Q

Meningocele

A

herniation of meninges in cranium bifidum or spina bifida

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27
Q

Meningoencephalocele

A

Herniation of meninges and brain in cranium bifidum

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28
Q

Herniation of spinal cord and meninges in spina bifida

A

meningomyelocele

29
Q

Most common brain malformation with BVD

A

Cerebellar hypoplasia (also with feline panleuk, hog cholera, parvovirus)

30
Q

Underlying cause of storage diseases

A

Lysosomal enzyme defects - defective catabolism

31
Q

What happens to cells that accumulate substrate in storage diseases

A

Cells will swell and can necrose, interferes with cell function

32
Q

How are storage diseases inherited

A

Autosomal recessive

33
Q

When do storage diseases present

A

Early, rapidly progressive and fatal

34
Q

How are storage diseases named

A

According to molecule whose degradation is defective

35
Q

Which CNS cells are most prone to ischemia

A

Neurons and oligodendroglia (highest metabolic rate)

36
Q

What matter is more sensitive than which to ischemia

A

Grey more sensitive than white

37
Q

Causes of polioencephalomalacia

A

high sulfur intake, thiamine deficiency or thiamine metabolism disturbance

38
Q

Where are polioencephalomalacia lesions

A

Softening of grey matter of cerebral cortex

39
Q

Leukoencephalomalacia causes

A

Moldy corn intake for over a month- fumonisin from fusarium

40
Q

Leukoencephalomalacia lesion location

A

Cerebral white matter necrosis

41
Q

Lesions of indirect salt poisoning

A

Cerebral edema, laminar cortical necrosis, eosinophilic meningoencephalitis

42
Q

Cause of indirect salt poisoning

A

Hihg salt diet and sudden restricted water intake - swine

43
Q

Ways bacterial infections get to CNS

A

septicemia, septic emboli from endocarditis, direct invasion, hematogenous spread

44
Q

Direct invasion routes of bacterial infection

A

Cribiform plate or middle ear

45
Q

Listeriosis common species

A

Ruminants

46
Q

Listeriosis causative agent

A

listeria monocytogenes in heavy feeding of silage

47
Q

Listeriosis characteristic lesions and locations

A

brainstem (medulla and pons) - microabscess (often in a focus of microgliosis)

48
Q

Pathogenesis of encephalitis

A

Bacteria spread up the motor and sensory branches of trigeminal nerve

49
Q

thrombotic meningoencephalitis species (infectious TME)

A

Cattle and sheep (young cattle in feed lots)

50
Q

Causative agent of thrombotic meningoencephalitis (infectious TME)

A

hisophilus somni

51
Q

Pathogenesis of development of CNS lesions of thrombotic meningoencephalitis (infectious TME)

A

Septicemia leads to cerebral vasculitis with hemorrhage, necrosis and thrombosis

52
Q

thrombotic meningoencephalitis (infectious TME) lesions

A

Mulitfocal hemorrhage and necrosis grossly, vasculitis, thombosis, infarction, netropphilic meningoencephalitis

53
Q

Histo features of viral infection

A

Non-suppurative meningoencephalities, peri-vascular cuffing, gliosis, +/- viral inclusions and neuronal degeneration/necrosis

54
Q

Cause of pseudorabies

A

Porcine herpesvirus 1

55
Q

Species affected by pseudorabies

A

All common domestic species

56
Q

CS of pseudorabies

A

Pigs- mild fever, no pruritis; non-pigs- intense pruritis, high mortality, fever, neuro signs; young pigs- mortality, convulsions, treamor/twitching, abortion, mummified fetus

57
Q

CS of CAE

A

Caprine arthritis encephalitis virus - hind limb ataxia to paresis or paralysis, can be fatal

58
Q

When is neuro disease observed with CAE or visna maedi

A

2-4 months, >2 years respectively

59
Q

Lesions of CAE/visna maedi

A

CAE- non-supp encephalo
VM: non-supp meningoenceph

both in white matter, both have demyelination

60
Q

Species affected by cryptococcus neoformans

A

cats, dogs horses

61
Q

How does crypto get to the brain

A

Nasal or sinus infection through cribiform or hematogenously through pulmonary infection

62
Q

Crypto histo lesions

A

Grey, gelatinous foci in brain and meninges

63
Q

Cause of equine protozoal myelitis

A

Sarcocystis neurona

64
Q

Why arent equine protozoal myelitis organisms not seen

A

ponazuril deowrming usually gets them before patho

65
Q

Causes of TSEs

A

Abnormal isoform (PrP-sc) of normal prion protein (PrP-c)

66
Q

How do animals acquire TSEs

A

Horizontal trasmission from consumption of infected feed

67
Q

Lesions of TSEs

A

intracytoplasmic neuronal vacuolation, astrocytosis

68
Q

Static vs dynamic stenosis in wobbler syndrome

A

Static- No matter what position the head or neck are in, the lesion is compressive. Dynamic- The spinal cord will only be compressed during flexion.

Pathology (5 decks)

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