L8: Path of the Nervous System (Farina)

Question 1

encephalo-

Answer 1

prefix for brain

Question 2

myelo-

Answer 2

prefix for white matter

Question 3

polio-

Answer 3

prefix for grey matter

Question 4

Nissl substance

Answer 4

cytoplasmic basophilic granular material (rER and polysomes)

Question 5

myelin made by:

Answer 5

Schwann cells in the periphery, oligodendrocytes in the CNS

Question 6

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

Answer 6

:)

Question 7

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

Answer 7

:)

Question 8

ependymal cells

Answer 8

line ventricles

Question 9

choroid plexus

Answer 9

• within ventricles
• produces CSF
• papillary-like structure

Question 10

oligodendrocytes

Answer 10

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

Question 11

3 types of glial cells

Answer 11

non-neuronal epithelial cells that line CNS
oligodendrocytes
astrocytes
microglia

Question 12

astrocytes

Answer 12

• 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

Question 13

microglia

Answer 13

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

Question 14

Gitter cells

Answer 14

• phagocytic cells of the nervous system

- derived from microglia or monocytes

Question 15

neuronophagia

Answer 15

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

Question 16

Wallerian degeneration

Answer 16

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

Question 17

Wobblers

Answer 17

axonal damage from narrowing of spinal cord

Question 18

spheroids

Answer 18

focal axonal swellings filled with degenerate organelles

Question 19

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

Answer 19

:)

Question 20

Astrocytosis

Answer 20

• 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

Question 21

gemistocytic astrocytes

Answer 21

plump, reactive astrocytes w/ eosinophilic cytoplasm

Question 22

3 types hydrocephalus

Answer 22

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

Question 23

microencephaly

Answer 23

abnormally small brain

Question 24

hydranencephaly

Answer 24

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

Question 25

porencephaly

Answer 25

cystic cavitation of the brain, usually involving cerebral white matter

Question 26

lissencephaly

Answer 26

brain lacks normal gyri and sulci | -normal in rodents, non-mammals

Question 27

dysraphia (neural tube closure defects)

Answer 27

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

Question 28

meningocele

Answer 28

herniation of meninges

Question 29

meningoencephalocele

Answer 29

herniation of meninges and brain/spinal cord

Question 30

viral causes of malformations

Answer 30

``` BVD feline panleukopenia hog cholera canine parvo border disease ```

Question 31

veratrum californicum ingestion -->

Answer 31

cyclopia

Question 32

storage diseases

Answer 32

Accumulation of substances in cells - usually due to defective catabolism - usually a result of a defect in lysosomal enzymes** - usually autosomal recessive, progressive, fatal

Question 33

How are storage diseases named?

Answer 33

according to the substrate that has defective degradation - Sphingolipidoses - Glycoproteinoses - Mucopolysaccharidoses - Glycogenoses - Ceroid lipofuscinoses

Question 34

Sphingolipidoses has defective degradation of what substrate?

Answer 34

molecules that form cell membranes

Question 35

Glycoproteinoses has defective degradation of what substrate?

Answer 35

carbohydrate component of N-linked glycoproteins

Question 36

Mucopolysaccharidoses has defective degradation of what substrate?

Answer 36

glycosaminoglycans

Question 37

Glycogenoses has defective degradation of what substrate?

Answer 37

glycogen

Question 38

Ceroid lipoguscinoses has defective degradation of what substrate?

Answer 38

lipofuscin | -"wear and tear" pigment which accumulates in old age

Question 39

what most sensitive to ischemia?

Answer 39

- neurons and oligodendroglia - grey matter more sensitive than white matter - vascular occlusive lesions rare in domestic animals

Question 40

neonatal maladjustment syndrome of foals

Answer 40

- "dummy foals" - presumed to be due to ischemia and reperfusion - lesions: laminar neuronal necrosis, multifocal small hemorrhages

Question 41

malacia

Answer 41

necrosis of the CNS

Question 42

Polioencephalomalacia

Answer 42

- 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

Question 43

thiamine deficiency

Answer 43

- 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

Question 44

CS of DIRECT salt poisoning (ingestion of excessive salt)

Answer 44

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

Question 45

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

Answer 45

- blindness, deafness, head pressing, convulsions | - lesions: cerebral edema, laminar cortical necrosis, nonsuppurative and eosinophilic meningoencephalitis

Question 46

Nigropallidal encephalomalacia in horses

Answer 46

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

Question 47

Leukoencephalomalacia in horses

Answer 47

- 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

Question 48

Lead poisoning

Answer 48

- 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

Question 49

Malacic diseases (causing necrosis of CNS)

Answer 49

``` Polioencephalomalacia Thiamine def. Salt poisoning Nigropallidal encephalomalacia Leukoencephalomalacia Lead poisoning ```

Question 50

malformations of the CNS

Answer 50

``` hydrocephalus Microencephaly Hydranencephaly Porencephaly Lissencephaly Disraphia Prosencephalic hypoplasia Cranium bifidum and meningoencephalocele Spina bifida ```

Question 51

Ischemic lesions

Answer 51

infarct | neonatal maladjustment syndrome of foals