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Systemic Pathology (Spring 2015) > L8: Path of the Nervous System (Farina) > Flashcards

L8: Path of the Nervous System (Farina) Flashcards

1
Q

encephalo-

A

prefix for brain

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2
Q

myelo-

A

prefix for white matter

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3
Q

polio-

A

prefix for grey matter

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4
Q

Nissl substance

A

cytoplasmic basophilic granular material (rER and polysomes)

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5
Q

myelin made by:

A

Schwann cells in the periphery, oligodendrocytes in the CNS

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6
Q

dura mater = outermost layer of meninges (periosteum outermost later in brain)

A

:)

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7
Q

pia mater is vascular and lies next to spinal cord/white matter

A

:)

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8
Q

ependymal cells

A

line ventricles

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9
Q

choroid plexus

A
  • within ventricles
  • produces CSF
  • papillary-like structure
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10
Q

oligodendrocytes

A

-form myelin that wraps around axons in the CNS (same as Schwann cells in the PNS)**

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11
Q

3 types of glial cells

A

non-neuronal epithelial cells that line CNS
oligodendrocytes
astrocytes
microglia

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12
Q

astrocytes

A
  • type of glial cell
  • star-shaped cells w/ special stains (ie. GFAP immunostain)
  • have elaborate cell processes that form the BBB**
  • secrete paracrines that promote tight junction formation
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13
Q

microglia

A
  • type of glial cell
  • phagocytic cells
  • have small nuclei with relatively little cytoplasm
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14
Q

Gitter cells

A
  • phagocytic cells of the nervous system

- derived from microglia or monocytes

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15
Q

neuronophagia

A

phagocytes (microglia) gather around a necrotic neuron and phagocytose it to remove the debris
-char. of viral infections

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16
Q

Wallerian degeneration

A

focal damage to a myelinated axon results in degeneration of the axon segment distal to the site of damage
-Swiss cheese appearance

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17
Q

Wobblers

A

axonal damage from narrowing of spinal cord

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18
Q

spheroids

A

focal axonal swellings filled with degenerate organelles

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19
Q

liquefactive necrosis seen with ischemic injury in the CNS (ie. infarct)

A

:)

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20
Q

Astrocytosis

A
  • increase in size and number of astrocytes in response to injury
  • repair after CNS injury is largely the job of astrocytes (take role of fibroblasts in the brain)
  • occurs in Alzheimer’s
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21
Q

gemistocytic astrocytes

A

plump, reactive astrocytes w/ eosinophilic cytoplasm

22
Q

3 types hydrocephalus

A

1) Internal: fluid in ventricles
2) External: fluid in arachnoid space
3) communicating: fluid in ventricles and arachnoid space
* brachiocephalics prone*
* can be acquired*

23
Q

microencephaly

A

abnormally small brain

24
Q

hydranencephaly

A

near complete or complete absence of the cerebral hemispheres, leaving fluid-filled sacs by the meninges filled with CSF

25
Q

porencephaly

A

cystic cavitation of the brain, usually involving cerebral white matter

26
Q

lissencephaly

A

brain lacks normal gyri and sulci

-normal in rodents, non-mammals

27
Q

dysraphia (neural tube closure defects)

A

anencephaly: absence of brain
prosencephalic hypoplasia: absence of the cerebral hemispheres w/ preservation of the brainstem
cranium bifidum/spina bifida: dorsal midline defect through which the brain/spinal cord and meninges can protrude

28
Q

meningocele

A

herniation of meninges

29
Q

meningoencephalocele

A

herniation of meninges and brain/spinal cord

30
Q

viral causes of malformations

A 
BVD
feline panleukopenia
hog cholera
canine parvo
border disease
31
Q

veratrum californicum ingestion –>

A

cyclopia

32
Q

storage diseases

A

Accumulation of substances in cells

  • usually due to defective catabolism
  • usually a result of a defect in lysosomal enzymes**
  • usually autosomal recessive, progressive, fatal
33
Q

How are storage diseases named?

A

according to the substrate that has defective degradation

  • Sphingolipidoses
  • Glycoproteinoses
  • Mucopolysaccharidoses
  • Glycogenoses
  • Ceroid lipofuscinoses
34
Q

Sphingolipidoses has defective degradation of what substrate?

A

molecules that form cell membranes

35
Q

Glycoproteinoses has defective degradation of what substrate?

A

carbohydrate component of N-linked glycoproteins

36
Q

Mucopolysaccharidoses has defective degradation of what substrate?

A

glycosaminoglycans

37
Q

Glycogenoses has defective degradation of what substrate?

A

glycogen

38
Q

Ceroid lipoguscinoses has defective degradation of what substrate?

A

lipofuscin

-“wear and tear” pigment which accumulates in old age

39
Q

what most sensitive to ischemia?

A
  • neurons and oligodendroglia
  • grey matter more sensitive than white matter
  • vascular occlusive lesions rare in domestic animals
40
Q

neonatal maladjustment syndrome of foals

A
  • “dummy foals”
  • presumed to be due to ischemia and reperfusion
  • lesions: laminar neuronal necrosis, multifocal small hemorrhages
41
Q

malacia

A

necrosis of the CNS

42
Q

Polioencephalomalacia

A
  • sometimes assoc. with a high sulfur** intake
  • a def. in thiamine or disturbance in thiamine metabolism also implicated
  • occasionally observed in cases of water deprivation
  • ruminants
43
Q

thiamine deficiency

A
  • required for carnivores
  • seen in fox, cat, mink consuming fish or horse consuming plants containing a thiaminase
  • CS: ataxia, neck ventroflexion, incoordination, mydriasis, convulsions
  • Lesions: hemorrhage, necrosis and neuropil vacuolation in periventricular grey matter
44
Q

CS of DIRECT salt poisoning (ingestion of excessive salt)

A
  • mainly affects cattle
  • v/d, paresis, blindness, abdominal pain
  • congestion of abomasal mucosa, dark watery intestinal contents, NO CNS lesions
45
Q

CS/lesions of INDIRECT salt poisoning (ingestion of high salt diet + restrictred water intake for several days)

A
  • blindness, deafness, head pressing, convulsions

- lesions: cerebral edema, laminar cortical necrosis, nonsuppurative and eosinophilic meningoencephalitis

46
Q

Nigropallidal encephalomalacia in horses

A
  • due to ingestion of yellow star thistle and Russian knapweed
  • putative neurotoxin causes glutathione depletion
  • malacia in the globus pallidus and substantia nigra**
47
Q

Leukoencephalomalacia in horses

A
  • caused by moldy corn consumption for at least 1 mo.
  • toxin = fumonisin
  • CS: circling, visual impairment, weakness, pharyngeal paralysis, death
  • lesion: necrosis of the cerebral white matter
48
Q

Lead poisoning

A
  • most common in cattle
  • CS: staggering, m. tremor, convulsion, head pressing, blindness, hypersalivation, ruminal atony, recumbency, hyperesthesia, death
  • lesions in cattle: only seen if dz course is at least several days; laminar cerebral cortical necrosis
  • lesions in dogs: white matter edema in brain/spinal cord, demyelination
49
Q

Malacic diseases (causing necrosis of CNS)

A 
Polioencephalomalacia
Thiamine def.
Salt poisoning
Nigropallidal encephalomalacia
Leukoencephalomalacia
Lead poisoning
50
Q

malformations of the CNS

A 
hydrocephalus
Microencephaly
Hydranencephaly
Porencephaly
Lissencephaly
Disraphia
Prosencephalic hypoplasia
Cranium bifidum and meningoencephalocele
Spina bifida
51
Q

Ischemic lesions

A

infarct

neonatal maladjustment syndrome of foals

Systemic Pathology (Spring 2015) (10 decks)

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