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Pathology > Lecture: Path of neuro syst (Farina) > Flashcards

Lecture: Path of neuro syst (Farina) Flashcards

1
Q

Encephalo-

A

Prefix for brain

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2
Q

Myelo-

A

Prefix for spinal cord

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3
Q

Leuko-

A

Prefix for white matter

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4
Q

Polio-

A

Previx for grey matter

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5
Q

Grey matter location

A

Where the neurons are

  • peripherally in cerebral and cerebellum
  • All the nuclei
  • columns of spinal cord
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6
Q

White matter

A

Bundles of myelinated axons

  • cortex of cerebrum and cerebellum
  • peripherally in spinal cord
  • mixed in some of gray matter
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7
Q

Neuropil

A
  • all the matter in between glial cells and neurons
  • only in grey matter
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8
Q

Nissl substance

A
  • cytoplasmic basophilic granular material
    • rER
    • polysomes
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9
Q

Axons special stain

A

Silver stain

black lines are axons

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10
Q

Myelin

Special stain

A
  • Surrounds some of the axons
  • clear areas around little dots

*Special stain to look for demyelination: Luxol fast blue stain

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11
Q

Meninges

Layers of Meninges

A
  • Covering of brain and spinal cord
    • Outermost layer: dura mater (periosteum of skull)
    • Middle layer: arachnoid
    • Inner later: Pia mater (vascular layer)
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12
Q

Lepto meninges

A

arachnoid plus pia mater

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13
Q

Ependymal cells

A
  • Ciliated cuboidal cells that line ventricles
  • Helps the flow of CSF
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14
Q

Choroid plexus

A
  • Papillary structure in ventricles
  • Lined by epithelial cells
  • Produces CSF

*Some inflammatory cells in Choroid plexus is ok

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15
Q

Glial cells

A
  • Oligodendrocytes:
    • form myelin that wraps around axons in CNS
    • Same as Schwann cells in PNS
  • Astrocytes:
    • star-shaped cells with special stains
    • have elaborate cell processes that form the BBB
  • Microglia:
    • phagocytic cells
    • small nuclei, relatively little cytoplasm
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16
Q
A
  • Glial cells are the tiny dense cells
  • Astrocytes are a little larger nuclei and more open chromatin
  • Oligadendracytes are smaller with denser nuclei
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17
Q
A
  • Astrocyte
    • wrap around blood vessels forming foot processes that make up the BBB
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18
Q

Gitter cells

A
  • Phagocytic cells of the nervous system
  • derived from microglia or monocytes
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19
Q

Central chromatolysis

A
  • Degenerative change
  • Swollen neuron
    • eosinophilic
    • dispersion of nissel substance
    • nucleus pushed to side
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20
Q

Neuronal necrosis

A
  • Red is dead
  • Neurons usually have basophilic cytoplasm, eosinophilic is bad (dead)
    • pyknosis, karyorexus, karyolysis
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21
Q

Neuronophagia

Characteristic of….

A
  • Phagocytes (microglia) gather arond a necrotic neuron and phagocytose it to remove debris
  • Characteristic of viral infections
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22
Q

Wallerian degeneration

Results in….

Characteristic of…..

A
  • Focal damage to a myelinated axon
  • Results in degeneration of the axon segment distal to site of damage
  • Characteristic of compressive lesons (IVDD) (wobblers in a horse)
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23
Q
A
  • Wallerian degeneration
    • Swollen/empty myelin sheaths
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24
Q

Wallerian degeneration

The little caterpillars are…

A
  • Digestion chambers
    • Gitter cells come in and eat degenerate axons
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25
Q
A

Gitter cells in digestion chambers

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26
Q

Spheroids

A
  • Degenerate axons
  • foxal axonal swellings
  • big eosinophilic swelling filled with degenerate organelles
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27
Q

Liquefactive necrosis

Typical injuries

End result…

A
  • Lose cell outlines
  • Ischemic lesions
  • abcesses with lots of proteolytic enzymes
  • first area looks squishy, end result is a hole
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28
Q

Coagulative necrosis

A
  • Maintains cell outlines
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29
Q

Fibroblasts

A
  • Can’t repair brain because there are no fibroblasts in the brain
  • There are fibroblasts in meninges
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30
Q
A

Liquefactive necrosis

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31
Q
A
  • Liquefactive necrosis are the holes (spots with no tissue)
32
Q

Astrocytosis

A
  • Inc in size and number of astrocytes in response to injury
  • Repair after CNS injury is largely job of astrocytes
    • swell and divide and cell processes proliferate
33
Q
A
  • Reactive astrocytes
    • purple cells with swollen cytoplasm in middle
34
Q

Gemistocytosis

A
  • Plump, reactive astrocytes with eosinophilic cytoplasm
  • Nuclei are NOT necrotic
35
Q

Alzheimer’s type II astrocytes

A
  • Typical of hyperammonnemia
  • Enlarged, vesicular nuclei, typical of hepatic encephalopathy
  • Large nuclei with open chromatin pattern
  • Flank the neurons in the cerebral cortex
36
Q

Hydrocephalus

3 types

Most common in….

Can be…

A
  • Internal:
    • Fluid in ventricles
    • Most common type
  • External:
    • fluid in arachnoid space
  • Communicating:
    • fluid in ventricles and arachnoid space

*Most common in brachycephalic breeds

*Can be acquired: CSF flow blockage

37
Q
A
  • Hydrocephalus
  • Brain should not look like a deflated party balloon
38
Q

Microencephaly

A
  • Abnormally small brain
  • Usually cerebrum
39
Q

Hydranencephaly

A
  • Near complete or complete abscence of cerebral hemispheres
  • Leaves fluid-filled sacs formed by meninges filled with CSF
40
Q

Porencephaly

A
  • Cystic cavitation of the brain
  • Usually involving cerebral white matter
  • thought to be in-utero infarcts
41
Q

Lissencephaly

Normal Lissencephalic animals

Posterchild in dogs…

A
  • No Gyri and Sulci in brain (flat brain)
  • Species that don’t have gyri and sulci
    • rodents
    • rats
    • bats
    • Marmosets and tamarins
    • non-mammals

*Lhaso Apso’s poster children

42
Q

Dysraphia: definition

Types of defects…

A
  • Neural tube closure defects
  • Types of defects
    • Anencephaly: abscence of the brain
    • Prosencephalic hypoplasia: absence of cerebral hemispheres w/ preservation of brainstem
    • Cranium bifidum/spina bifida: dorsal midline defect through which brain/spinal cord and meninges can protrude
      • meningocele: herniation of meninges
      • meningoencephalocele/meningomyelocele: herniation of meninges and brain/spinal cord
43
Q
A

Prosencephalic hypoplasia

  • cerebellum and brainstem
44
Q
A
  • Foal with Prosencephalic hypoplasia, almost anencephaly
45
Q
A
  • Cranium bifidum and meningoencephalocele
  • Brain and meninges are up in the defect
46
Q
A
  • Cranium bifidum and meningocele with age match control
47
Q
A
  • Spina bifida
48
Q

Viral causes of malformations

Classic culprits..

A
  • BVD: d. 100-170 of gestation
    • usually cerebellar hypoplasia
  • Feline panleukopenia
  • Hog cholera (classical swine fever)
  • Canine Parvovirus
  • Border disease (sheep)

*Parvoviruses and Pestiviruses are classic culprits

49
Q

Cyclopia (synopthalmus)

A
  • Veratrum californicum ingestion on or about day 14
  • Usually sheep
50
Q

Storage Diseases

Most are….conditions

A
  • Accumulation of substances in cells
  • Usually due to defective catabolism: defect in lysosomal enzymes
  • Tissues which accumulate the substance are those most active in turning over substrate
  • Usually autosomal recessive conditions
    • ​neuro signs early in life
    • typically progressive and fatal
51
Q

Storage diseases names according to:

Examples…

A
  • Substrate that has defective degradation
  • Examples
    • Sphingolipidoses: molecules that form cell membranes
    • Glycoproteinoses: carbohydrate component of N-linked glycoproteins
    • Mucopolysaccharidoses: glycosaminoglycans
    • Glycogenoses: glycogen
    • Ceroid lipofuscinoses: lipofuscin
52
Q
A
  • Ceroid lipofuscinosis
    • tan stuff is lipofuscin
53
Q
A
  • GM2 gangliosidosis (Tay Sachs disease)
54
Q

Tissues most sensitive to Ischemic lesions….

Examples:

Vascular occlusions in domestic animals are…

A
  • Tissues with high metabolic requirements
  • Neurons and oligodendroglia most sensitive to ischemia
  • Grey matter is more sensitive than white matter
  • Vascular occlusive lesions are rare in domestic animals
55
Q
A

Infarct (looks squishy and red)

Histologically: pale region is the necrotic region

56
Q

Neonatal maladjustment syndrome of foals

(dummy foals)

Histologically:

A
  • Presumed to be due to ischemia and reperfusion
  • Lesions
    • laminar neuronal necrosis
    • multifocal small hemorrhages
  • Histologically:
    • laminar cortical necrosis
    • most foals make it ok tho
57
Q

Malacic diseases

Definition

A

Softening => usually means CNS necrosis

58
Q

Polioencephalomalacia

Def

Associations

Often seen in…

A
  • Def
    • softening of the grey matter of the brain
  • Associated with
    • high sulfur intake
    • deficiency in thiamine or disturbance in thiamine metabolism
    • occasionally observed in cases of water deprivation
  • Often seen in ruminants
59
Q
A
  • Polioencephalomalacia
    • only normal grey matter is at the bottom
    • fluoresces under UV light
60
Q
A
  • Polioencephalomalacia
  • fragmented and necrotic
61
Q

Thiamine deficiency

A
  • Thiamine (Vitamin B1) is a dietary requirement in carnivores
  • Some fish have a thiaminase
  • Horses can consume plants (Bracken fern and horsetail) that have a thiaminase
62
Q

Thiamine deficiency

CS

Lesion

A
  • CS
    • ataxia
    • neck ventroflexion
    • incoordination
    • mydriasis
    • convulsions
  • Lesions
    • hemorrhage
    • necrosis
    • neuropil vacuolation in periventricular grey matter
63
Q

Salt poisoning

Direct

Animal commonly affected

CS

Lesion

A
  • Direct
    • too much salt ingestion (high salinity in drinking water)
  • Mainly affects cattle
  • CS
    • vomiting
    • diarrhea
    • paresis
    • blindness
    • abdominal pain
  • Lesions
    • Congestion of abomasal mucosa
    • dark water intestinal contents
    • NO CNS LESIONS
64
Q

Salt poisoning

Indirect

CS

Lesions

Usually affects…

A
  • Ingestion of a high salt diet (>/= 2%) in addition to dec water intake
  • CS
    • blindness
    • deafness
    • head pressing
    • convulsions
  • Lesions
    • Cerebral edema
    • laminar cortical necrosis
    • nonsuppurative and eosinophilic meningoencephalitis
  • Usually affects pigs
65
Q

Eosinophils usually….

A

parasite related

66
Q
A

Salt poisoning

  • gyri and sulci may look flattened from being squished up against the skull
  • Cerebellar coning/herniation
67
Q
A
  • Salt poisoning
  • red, eosinophilic, necrotic neurons
68
Q

Non-supporative

A

No neutraphils

69
Q

Nigropallidal encephalomalacia in horses

Cause

Toxin

Result

A
  • Cause
    • ingestion of yellow star thistle (Centaurea solstitialis) and Russian knapweed (Centaurea repens)
  • Toxin
    • repin-sesquiterpene lactone => causes glutathione depletion
  • Result
    • Malacia in the blobus pallidus and substantia nigra
70
Q
A
  • Nigropallidal encephalomalacia
  • bilaterally symmetrical holes in the brain
71
Q

Leukoencephalomalacia in horses

Cause

CS

Lesion

A
  • Cause
    • moldy corn consumption for >/= 1 month
      • toxin: fumonisin produced by Fusarium moniliforme
    • CS
      • Circling
      • Somnolence
      • visual impairment
      • weakness
      • pharyngeal paralysis
      • usually death 2-3 days after onset of clinical signs
    • Lesion
      • necrosis of cerebral white matter
72
Q
A
  • Leukoencephalomalacia
  • Necrotic white matter
  • Holes in the histologic section are bad
73
Q
A
  • Leukoencephalomalacia
    • vacuolization, hemorrhage, necrosis
74
Q

Lead poisoning

A
  • Most common in Cattle
    • also seen in sheep, dogs, and horses
  • Cattle usually acquire lead from paint or batteries
  • Dogs usually acquire lead from drinking leaded gasoline
75
Q

Lead poisoning

CS in cattle

Lesions in cattle

Lesions in dogs

Clinically looks like…

A
  • CS in cattle
    • staggering
    • muscle tremors
    • convulsions
    • head pressing
    • blindness
    • hypersalivation
    • ruminal atony
    • recumbency
    • hyperesthesia (to touch and sound)
    • death
  • Lesions in cattle
    • laminar cerebral cortical necrosis if disease course longer than several days
  • Lesion in dogs
    • White matter edema in brain and spinal cord
    • demyelination

*Clinically looks like rabies

Pathology (6 decks)

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