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

Lecture: Path of neuro syst (Farina) Flashcards

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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
Gitter cells in digestion chambers
26
Spheroids
* Degenerate axons * foxal axonal swellings * big eosinophilic swelling filled with degenerate organelles
27
Liquefactive necrosis Typical injuries End result...
* Lose cell outlines * Ischemic lesions * abcesses with lots of proteolytic enzymes * first area looks squishy, end result is a hole
28
Coagulative necrosis
* Maintains cell outlines
29
Fibroblasts
* Can't repair brain because there are no fibroblasts in the brain * There are fibroblasts in meninges
30
Liquefactive necrosis
31
* Liquefactive necrosis are the holes (spots with no tissue)
32
Astrocytosis
* 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
* Reactive astrocytes * purple cells with swollen cytoplasm in middle
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Gemistocytosis
* Plump, reactive astrocytes with eosinophilic cytoplasm * Nuclei are NOT necrotic
35
Alzheimer's type II astrocytes
* Typical of hyperammonnemia * Enlarged, vesicular nuclei, typical of hepatic encephalopathy * Large nuclei with open chromatin pattern * Flank the neurons in the cerebral cortex
36
Hydrocephalus 3 types Most common in.... Can be...
* 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
* Hydrocephalus * Brain should not look like a deflated party balloon
38
Microencephaly
* Abnormally small brain * Usually cerebrum
39
Hydranencephaly
* Near complete or complete abscence of cerebral hemispheres * Leaves fluid-filled sacs formed by meninges filled with CSF
40
Porencephaly
* Cystic cavitation of the brain * Usually involving cerebral white matter * thought to be in-utero infarcts
41
Lissencephaly Normal Lissencephalic animals Posterchild in dogs...
* 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
Dysraphia: definition Types of defects...
* 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
Prosencephalic hypoplasia * cerebellum and brainstem
44
* Foal with Prosencephalic hypoplasia, almost anencephaly
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* Cranium bifidum and meningoencephalocele * Brain and meninges are up in the defect
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* Cranium bifidum and meningocele with age match control
47
* Spina bifida
48
Viral causes of malformations Classic culprits..
* 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
Cyclopia (synopthalmus)
* Veratrum californicum ingestion on or about day 14 * Usually sheep
50
Storage Diseases Most are....conditions
* 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
Storage diseases names according to: Examples...
* 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
* Ceroid lipofuscinosis * tan stuff is lipofuscin
53
* GM2 gangliosidosis (Tay Sachs disease)
54
Tissues most sensitive to Ischemic lesions.... Examples: Vascular occlusions in domestic animals are...
* 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
Infarct (looks squishy and red) Histologically: pale region is the necrotic region
56
Neonatal maladjustment syndrome of foals (dummy foals) Histologically:
* 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
Malacic diseases Definition
Softening =\> usually means CNS necrosis
58
Polioencephalomalacia Def Associations Often seen in...
* 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
* Polioencephalomalacia * only normal grey matter is at the bottom * fluoresces under UV light
60
* Polioencephalomalacia * fragmented and necrotic
61
Thiamine deficiency
* 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
Thiamine deficiency CS Lesion
* CS * ataxia * neck ventroflexion * incoordination * mydriasis * convulsions * Lesions * hemorrhage * necrosis * neuropil vacuolation in periventricular grey matter
63
Salt poisoning Direct Animal commonly affected CS Lesion
* 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
Salt poisoning Indirect CS Lesions Usually affects...
* 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
Eosinophils usually....
parasite related
66
Salt poisoning * gyri and sulci may look flattened from being squished up against the skull * Cerebellar coning/herniation
67
* Salt poisoning * red, eosinophilic, necrotic neurons
68
Non-supporative
No neutraphils
69
Nigropallidal encephalomalacia in horses Cause Toxin Result
* 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
* Nigropallidal encephalomalacia * bilaterally symmetrical holes in the brain
71
Leukoencephalomalacia in horses Cause CS Lesion
* 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
* Leukoencephalomalacia * Necrotic white matter * Holes in the histologic section are bad
73
* Leukoencephalomalacia * vacuolization, hemorrhage, necrosis
74
Lead poisoning
* 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
Lead poisoning CS in cattle Lesions in cattle Lesions in dogs Clinically looks like...
* 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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