Tissue Injury and Repair 4 Flashcards Preview

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Flashcards in Tissue Injury and Repair 4 Deck (26):
1

HEAD TRAUMA

Brain will move. Often see damage on opposite side as well as where brain was hit.
Axial, rotational and angular energy applied to the brain determine the severity of shear, tensile and compressive forces that cause neuronal and vascular injury.

2

MENINGES

Calvarium (skull)
Dura mater
Arachnoid mater
Subarachnoid space- contains fluid
Pia mater- in contact with brain.

DURA MATER MUST BE REMOVED FROM BRAIN AND SPINAL CORD BEFORE FIXATION, OR IT WILL NOT WORK.

3

BLOOD BRAIN BARRIER

Comprised of capillary endothelial cells, basement membrane, astrocytic foot processes.
Formed structurally by tight junctions between endothelial cells.
Formed functionally by specialised transport systems in these cells- only certain molecules are transported.

4

CORTICAL HAEMORRHAGE

In the cortex of the brain

5

SUBDURAL HAEMORRHAGE

Underneath the dura mater. Usually laceration of a vein- low pressure.

6

SUBARACHNOID HAEMORRHAGE

Haemorrhage beneath the arachnoid mater, in the subarachnoid space.

7

EPIDURAL HAEMORRHAGE

Outside the dura mater. Usually laceration of the meningeal artery- high pressure.

8

CONCUSSION

Degenerative changes to brainstem nuclei, becoming more severe if repeated.
No blood.

9

CONTUSION

More severe impact causes haematoma of subarachnoid space and/or parenchyma.
Could be caused by tumour.

10

BIRDS

Pooling of blood in venous sinuses of calvarium seen in response to trauma. Often seen as a post mortem change- there may be no actual damage to the skull or brain- check!

11

LACERATION

Torn by fractures or penetrating objects, including bone fragments, bullets.
As a general rule, acute nervous system injuries (such as laceration) are more disruptive than slowly developing injuries.

12

ASTROCYTES

Provide structural support.
Form part of blood brain barrier.
Selective transfer of neurotransmitters.
Fluid and ionic homeostasis.
Uptake of excess neurotransmitters.

Undergo hypertrophy and hyperplasia in response to injury. GLIOSIS.

13

BRAIN INJURY

There are very few fibrocytes in the brain, so it cannot form scar tissue.
Astrocytes and few fibrocytes try to form fibrosis.
Little fibrosis is with penetrating trauma or around abscesses.

Astrocytes are the principal cells responsible for repair and scar formation in the brain- GLIOSIS (increase in glial cells)

With large defects, there may be a persistent cavity formed.
Fibrocytes ARE present in the meninges, so fibrous scar tissue can form if the meninges is affected.

14

GEMISTOCYTIC ASTROCYTES

aka. GEMISTOCYTES.
Reactive astrocytes (seen in response to injury)

Long standing gliosis is more fibrillar.

15

MICROGLIA

'Macrophages of the brain'
make up <5% of glial cells.
Proliferate following injury, can transform in to brain macrophages.
Aggregates/clusters at small sites of injury are called microglial NODULES.

16

GITTER CELLS

Macrophages which have ingested degenerate myelin (nerve sheath) and other debris eg. in liquefied necrotic area.
Foamy cytoplasm.
Can persist for months.

17

SPINAL TRAUMA

Can be extrinsic or intrinsic.
EXTRINSIC- Cars, kicks, crushing injury, penetrating objects.
Fracture most likely to be seen at thoracolumbar junction.
INTRINSIC- Disc prolapse, pathological vertebral fractures (eg. due to abscess, neoplasia).
Intervertebral disc disease most likely to be seen around thoracolumbar area as there is little extradural space, and the thoracic cord is protected by conjugal ligaments.

18

INTERVERTEBRAL DISC DISEASE

Seen in CHONDODYSTROPHIC dogs as young as 6 months.
Nucleus pulposus is replaced by cartilage, which increases pressure on annulus fibrosis.
Annulua fibrosis degenerates, protrusion can occur.
Sudden protrusion is likely.

19

HANSEN TYPE I HERNIATION

Seen in chondodystrophic animals. Degenerative changes to the vertebral discs can be seen in animals as young as 6 months.
Cartilagenous nucleus pulposus is released from the annulus fibrosis and enters the spinal canal, where it compresses the spinal cord.

20

HANSEN TYPE II HERNIATION

Seen in NON-CHONDODYSTROPHIC animals.
Age related metaplasia of nucleus pulposus means it gradually loses it's elasticity.
This causes increased stress on the annulus fibrosis, which protrudes up in to the spinal canal, compressing the spinal cord.
Seen clinically by 8-10 years of age.

21

CERVICAL STENOTIC MYELOPATHY

Stenosis- narrowing.
Myelo- spinal cord.
Seen in horses due to malformation or malarticulation of cervical vertebrae.
Seen in young, rapidly growing breeds (dogs also- large breed, male, rapid growing. See both forms).
Neck can be submitted to pathologist for PM removal of spinal cord- should NOT be done in practice.
Two types are seen:
1. Cervical static stenosis.
2. Cervical vertebral instability.

22

CERVICAL STATIC STENOSIS

Narrowing of spinal canal due to bone formation.
Usually in horses aged 1-4 years.
Affects C5-C7

23

CERVICAL VERTEBRAL INSTABILITY

DYNAMIC- narrowing of the spinal canal is only seen when neck is flexed.
Usually in horses aged 8-18 months of age.
Affects C3-C5.

24

WALLERIAN DEGENERATION

Result of trauma, classically seen in compression.
Follows myelinated axonal disruption in the brain, spinal cord or nerves.
SEQUENCE OF DEGENERATION AND REMOVAL OF SEVERED AXONS.
First described in peripheral nerves.
Everything distal to the trauma degenerates and myelin is removed by phagocytosis- 'digestion chambers'.

Histologically- Digestion chambers containing myelin etc.
Axonal spheroid- swollen axon. Not always seen, but are a useful indicator.

25

REGENERATION?

After Wallerian degeneration, CNS axons do NOT regenerate.
Oligodendrocytes prevent axonal budding by providing myelin proteins (sheath) for up to 50 axons each.
No endoneurium (no fibrocytes).

26

PERIPHERAL NERVE REGENERATION

Peripheral nerves can regenerate.
SCHWANN CELLS are present instead of oligodendrocytes.
Endoneurium is present- this fibrous sheath round the axon acts as a scaffold if cell is damaged.

Schwann cells proliferate and bridge the gap caused by damage.
Must be closely apposed ( CONDUCTION VELOCITY OF NERVE IMPULSE IS SLOWER.