Tissue Injury & Repair 4: Nervous System Flashcards Preview

Pathology > Tissue Injury & Repair 4: Nervous System > Flashcards

Flashcards in Tissue Injury & Repair 4: Nervous System Deck (28):
1

If we were to put the brain in a fixative what should we do prior to that? 

Remove the dura mater from the brain as well as the spinal cord. 

2

What is the structural components of the blood brain barrier?

  1. Capillary endothelial cells
  2. Basement membrane
  3. Astrocytic foot processes. 

The basement membrane has these thin astrocytic foot process joining onto the blood vessels. 

 

Key component of the BBB is the forming of tight junctions between the endothelial cells which allows specialized transport systems in these cells. 

3

What are the different forms of head trauma (hemorrhage) than can occur in the brain? 

  1. Epidural hemorrahge: occurs outside of the dura mater and occurs when the meningeal artery has been severed.
  2. Subdural hemorrahge: occurs when the meningeal vein has been severed but this is less severe because there is less pressue involved since only the vein is lacerated.
  3. Subarachnoid hemorrahge
  4. Cortical hemorrahge
  5. Deep intracerebral hemorrahge
  6. hemorrahge in subcortical white matter

4

What is a concussion?

degenerative changes in brainstem nuclei, more severe if repeated. 

5

What is a contusion?

More severe impact. Hematoma in the subarachnoid space and or parenchyma. 

6

What is birds in regards to head trauma? 

Pooling of blood in venous sinuses of calvarium,  causing no damage to skull or brain. 

This is PM change rather than a hematoma. 

7

What is a laceration?

Torn by fractures or penetrating objects including bone fragments, bullets. 

8

What are astrocytes, where are they used, and what is their function?

  • Astrocytes have the foot processes that attach to the BM of the blood vessels in the brain. 
  • They provide structural support to the BBB.
  • They provide selective transfer of NT 
  • Maintain fluid and ion homeostasis
  • Uptake of excess NT's

 

 

9

Comment on the role of astrocytes during brain injury, why they are necessary, and their response during an injury. 

  • The brain cannot form scar tissue because it contains very few fibrocytes. Because of this limited fibrosis astrocytes are the main cells responsible for repair and scar formation it the brain = GLIOSIS v. Fibrosis. 
  • The meninges do have some fibroblasts so they will contribute to a fibrous capsule but primarily it is the astrocytes doing most of the repair. 
  1. When the brain is injured the astrocytes will respond by undergoing hypertrophy and hyperplasia. 
  2. The reactive astrocytes that provide this tissue repair and scarring are called GEMISTOCYTIC ASTROCTYES. 

10

 

What is this picture of?

Q image thumb

Gemitocytic astrocytes

11

Identifty these cells. What is their function? 

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  • Microglia cells- Macrophages of the brain.
  • They proliferate after injury and can transform into brain macrophages. 
  • Will form microglial nodules when aggregating at small sites of injury. 

12

Identify these cells. What is their role and function. What is a histological characteristic that can be identified. 

Q image thumb

  • Gitter cells- macrophages that have ingested degenerate myelin and other debris. 
  • Unique histo characteristic: FOAMY CYTOPLASM

13

What are some causes of extrinsic spinal trauma? Where is the most common fracture site during extrinsic spinal trauma?

  • Hit by car, Kicked, crushed, penetrating objects can all cause extrinsic spinal trauma.
  • Fractures most common about the TL junction. 

14

What are some causes of intrinsic spinal trauma? 

  • Disc prolapse
  • Pathological veterbral fractures (abscess, neoplasia)
  • Intervertebral Disc Disease- most debilitating at TL junction because there is little extradural space. 

15

What is intervertebral disc disease? 

  • Nucleus Pulposus replaced by chondroid tissue. Transforming from gel like substance to less elastic cartilage like substance. 
  • Annulus fibrosis surrounding the nucleus pulposus (now chondroid like) is places under increasing stress and is degenerating itself. 
  • Depending on type of protrusion could be HANSEN TYPE I OR TYPE II. 

16

What Chondrodystrophic breeds of dogs are prone to Intervertebral disc disease?

  • (Dachsund, Pekingnese): These breeds have degenerative changes genetically programmed usually beginning around 6 months of age. 
  • Eventually will get sudden protrusion (usually when jumping down from a couch) and the disc material will protrude into the spinal canal and compress the spinal cord. (Hansen type I)

17

What is nonchondrodystrophic Intervertebral disc disease?

  • Age related FIBROUS metaplasia of nucleus pulposus...gradually loses its elasticity.
  • (Note: In chondrodystrophic breeds it is a chondroid change the nucleus pulposus undergoes v. this case it is a fibrous change) 
  • Increased stress on the annulus fibrosis which protrudes into the spinal canal and compresses the spinal cord (Hansen type II)
  • Can begin to be noticed clinically at 8-10 yrs of age. 

18

What is Hansen Type I herniation?  What breeds does it occur in? 

  • Release of NUCLEUS PULPOSUS material into the spinal, resulting in spinal cord compression.
  • Chondrodystrophic breeds.
  • Get degeneration of annulus fibrosis therefore nucleus pulposus and protrude through. 

19

What is Hansen Type II herniation?

  • Protrusion of the annulus fibrosis into the spinal canal compressing the spinal cord. 
  • Annulus is still intact. 
  • Age related Interverterbal disc disease rather than breed related. 

20

What is cervial stenotic myelopathy? What species and age does this occur in?  What are the two types? If submitting the neck to the PM room how do you want to handle the specimen?

  • Occurs in young, rapidly growing large breed horses.
  • Malformation or malarticulation of cervical vertebra.
  1. Cervical static stenosis. 
  2. Cervial vertebral instability

PM submission: Take the muscle off, band saw off just lateral to midline of spinal cord to make sure spinal cord is intact and not ruined to see compression. 

21

What is cervical static stenosis? What age does it occur and what spinal segments?

Narrowing of spinal canal due to bone formation. 

Occurs in horses 1-4 years of age. 

Occurs at C5-C7.

22

What is Cervial Veterbral Instability? What age does this occur and what spinal segments?

  • Narrowing of the spinal cord only when the neck is flexed. Dynamic form v. static form with bone formation. 
  • Occurs in horses 8-18 months of age
  • C3-C5

23

Aside from horses, what other species (and breed of species) does Cervial Stenotic Myelopathy occur in? 

  • Dobermans
  • Great Danes
  • Rapid growht more frequent in males. 
  • Static and Dynamic forms. 

24

What is Wallerian Degeneration? 

  • process that results when a nerve fiber is cut or crushed, in which the part of the axon separated from the neuron's cell body degenerates distal to the injury
  • Once the myelinated axonal disruption occurs in the brain, spinal cord, or nerve, a sequence of degeneration and removal of severed axons occurs. 
  • The distal segment to the point of disruption will be degenerated and the meylin is removed by "Gitter Cells" via phagoyctosis. This is called a DIGESTION CHAMBER. 
  • The rest of the neuron will be fine because it has the neuronal cell body 
  • Occurs in the CNS & PNS

25

What are three main components that accompany Wallerian Degeneration? 

  1. Gitter cells
  2. Digestion Chamber which is gitter cell phagocytozing degenerative myelin.
  3. Axonal Spheroids (not always seen)

26

Identify this image.

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Digestion Chamber during Wallerian Degeneration. 

27

Identify this image. 

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Axonal Spheroid during Wallerian Degeneration. Not always seen. 

28

In regards to Wallerian Degeneration, what are some difference between CNS and PNS regeneration? 

Myelin is a phospholipid membrane that wraps around axons to provide them with insulation. It is produced by Schwann cells in the PNS, and by oligodendrocytes in the CNS. Myelin clearance is the next step in Wallerian degeneration following axonal degeneration. The cleaning up of myelin debris is different for PNS and CNS. PNS is much faster and efficient at clearing myelin debris in comparison to CNS, and Schwann cells are the primary cause of this difference.

 

CNS:

  • Axons DO NOT regenerate.
  • The myelin proteins (which produce the myelin sheath) produced from the oligodendrocytes in the CNS prevent axonal budding therefore preventing regeneration.
  • CNS DOES NOT HAVE AN ENDONEURIUM. 

 

PNS: 

  • Peripheral Nerves CAN regenerate.
  • Following damage, Schwann cells proliferate and bridge the gap (oligodendrocytes don't do this) however they must be closely opposed. (<1 cm) 
  • Schwann cells phagocytoze myelin, then extrude it then picked up my macrophages. 
  • Distal and proximal segements of the axon to the injury degenerate (Retrograde is back up towards the cell body, Anterograde- distal degeneration) 
  • The proximal stump will generate multiple sprouts and one sprout will take and continue to grow (very slowly) towards the NMJ to reinnervate the muscle. 
  • Once the regenerated axons reach the end organ, Schwann cells will begin to produe myelin. 
  • The NEW AXON has shorter internodal segements, is 80% of its original diameter, and the velocity of the nerve impluse is shorter. 
  • Endoneurium- fibrous sheat acts as a scaffold for regeneration