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Module 8 > Tissue Injury + Repair 1 > Flashcards

Tissue Injury + Repair 1 Flashcards

1
Q

what are the functions of neurons (3)

A
  1. transmission of impulses
  2. spatial and temporal interpretation of impulses
  3. 1inhibitory and stimulatory regulation of impulses
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2
Q

what are the function of astroglia

A
  1. regulation of extracellular neurotransmitter concentration
  2. fluid/electrolyte imbalances
  3. repair of injury (proliferation of processes)
  4. bundling of axons
  5. part of barrier system (glia limitans, BBB)
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3
Q

what is the function of oligodendroglia

A

myelination of axons in CNS

possible neuronal body homeostasis

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4
Q

what are the function of ependymal cells

A

movement of CSF through ventricular system

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5
Q

what is the function of the choroid plexus

A

secretion of CSF, barrier function (B-CSF-B)

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6
Q

what are the functions of microglia

A

immunosurveillance

immunoregulation

phagocytosis

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7
Q

what are the functions of the meningeal cells

A

barrier function (arachnoid-CSF-B)

subarachnoid CSF cushions brain

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8
Q

what are the functions of the endothelial cells

A

barrier function (BBB)

selective molecule tranport system

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9
Q

what are the cells involved with tissue injury and repair

A
  1. atroglia: repair of injury, part of barrier system (glia limitans, BBB)
  2. choroid plexus epithelial cells: barrier function (B-CSF-B)
  3. meningeal cells: barrier function (arachnoid-CSF-B)
  4. endothelial cells: barrier function BBB
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10
Q

what are the general concepts for understanding CNS injury (7)

A
  1. cells of CNS vary in susceptibility to injury: neurons –> oligodendrocytes –> astrocytes –> microglia –> blood vessels
  2. regeneration of neurons
  3. no or only very little regeneration of nerve fibres in CNS (better in PNS)
  4. fibroblasts only present in leptomeninges and CNS areas close to this –> astrocyte processes responsible for healing in deeper areas (however, break down much easier in fibrous tissue)
  5. brain cavity very full in physiological state –> if tissue/exudate added, something has to give (atrophy, displacement)

6. BBB (tight junction of endothelial cells + BM + astrocyte foot processes): can prevent antibodies, drugs and infectious causes from entering the brain; regulates extracellular compartment, movement from blood to CNS –> CNS isolated from biochemical changes

  1. CNS has fair ability to resist infection and injury. Once infected low degree of resistance compared to other tissues
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11
Q

what are the defence mechanisms of the CNS

A
  1. skin
  2. bony structures (calvarium/vertebrae)
  3. meninges, CSF
  4. barrier systems: BBB, B-CSF-B, glia limitans, arachnoid-CSF-B
  5. local innate immune system: microglia and astrocytes
  6. trafficking macrophages
  7. innate and adaptive immune system once BBB broken down
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12
Q

what is the neuron response to CNS tissue injury

A
  1. ischemic change (necrotic cell death) –> ischemia, bacterial toxins, inflammatory mediators, thermal injury, heavy metals, nutritional deficiencies (thiamine), trauma, ATP production decreased
  2. inclusion body formation
  3. cytoplasmic vacuolation (spongiform encephalopathy)
  4. central chromatolysis (dispersion of nissl substance –> axonal injury)
  5. intracytoplasmic deposition of material (storage disease, aging)
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13
Q

what are the responses of astrocytes to tissue injury

A
  1. swelling, hypertrophy, division, increased processes
  2. astrocytosis (increase in size + #)
  3. astrogliosis (hypertrophy –> more processes, ect. gemistocytes)
  4. formation of glial scar
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14
Q

what are oligodendrocytes response to tissue injury

A
  1. swelling, hypertrophy, degeneration (only precursors proliferate)
  2. satellitosis
  3. degeneration due to ischemia, viruses, lead, autoimmunity –> (primary) demyelination
  4. axonal injury leads to secondary demyelination
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15
Q

what are the ependymal and choroid plexus cells

A
  1. atrophy (ex. hydrocephalus), degeneration, necrosis
  2. no regeneration, instead astrogliosis
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16
Q

what are the responses of microglia to injury

A
  1. hypertrophy
  2. hyperplasia (glial nodules together with other cells)
  3. phagocytosis
  4. neuronophagia
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17
Q

what are the responses of meninges to injury

A

inflammatory changes (meningitis)

proliferation

mineralization

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18
Q

what are gitter cells

A

tissue necorsis

macrophages derived from blood monocytes

phagocytose lipid-laden debris –> foamy

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19
Q

what are the damages that can injure the CNS

A
  1. necrosis (any cell type)
  2. inflammation
  3. vascular changes (edema, swelling)
  4. gliosis –> proliferation of astrocytes, oligodendrocytes, microglia
  5. fibrosis (not really only astrocyte proliferation)
  6. severe inflammation –> severe tissue damage/necrosis (encephalomalacia)
  7. inflammation of CSF compartment –> obstruction of CSF flow –> hydrocephalus
  8. specific to axonal injury: Wallerian degeneration, central chromatolysis
  9. demyelination: primary and secondary
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20
Q

what is Wallerian degeneration

A

degeneration of axon (and dendritic processes) independently of neuronal cell body; CNS and PNS

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21
Q

what is the process of wallerian degeneration

A

anterograde degeneration with formation of axonal spheroids, distension of myelin sheaths, necrosis of axon and myelin sheaths, necrosis of axon and myelin sheaths and ingestion of both by macrophages (monocyte or microglial origin)

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22
Q

how does regeneration occur in the PNS with wallerian degeneration

A

formation of Bungner’s bands

axonal sprouting

segmental remyelination

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23
Q

what is the result of wallerian degeneration in the CNS

A

axonal loss and reactive astrogliosis (scar)

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24
Q

what are the damage to CNS

A
  1. vascular
  2. inflammatory (infection/immune-mediated)
  3. traumatic
  4. anomaly
  5. metabolic toxic
  6. iatrogenic/idiopathic
  7. neoplastic
  8. degenerative
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25
Q

what are vascular insults to CNS

A
  1. hemorrhage (focal)
  2. ischemia
26
Q

what are examples of hemorrhagic damages

A
  1. spontaneous
  2. hemorrhagic infarct
  3. vascular rupture (trauma)
  4. neoplastic origin
27
Q

what are ischemic insults

A

fibrocartilagenous emboli

common in dogs

clinically: peracute, often lateralized spinal cord signs with no pain

material thought to originate from nucleus puposus

28
Q

what is meningitis

A

inflammation of meninges

29
Q

what is encephalitis

A

inflammation of brain

(leukencephalitis = white matter, polioencephalitis = grey matter)

30
Q

what is myelitis

A

inflammation of spinal cord

31
Q

what are the types of inflammation

A
  1. suppurative: bacteria
  2. lymphocytic and histiocytic: viruses, protozoa
  3. granulomatous: fungi, protozoa, higher order bacteria (mycobacterium spp)
  4. eosinophilic: parasitic larval migration (salt poisoning in pigs)
32
Q

what are the portals of entry of inflammation infections

A
  1. direct extension
  2. hematogenous
  3. leukocyte trafficking
  4. retrograde axonal transport
33
Q

what occurs when a pathogen enters the brain

A
  1. inflammation
  2. disruption of BBB (hemorrhage and edema in addition)
34
Q

what is direct extension entry of a pathogen

A

penetrating injury

extension of nasal cavity/sinus infection via cribriform plate

extension of middle or inner ear infection

extension of osteomyelitis

35
Q

what is suppurative meningitis and ventriculitis

A

suppurative meningitis and ventriculitis

E. coli, salmonella spp, pasteurella, actinobacillus equuli, staphylococcus pyogenes, hemophilus parasuis

septicemia

capillary bed of meninges or choroid plexus

neonates

36
Q

what are brain abscesses

A

streptococcus spp (including strep. equi (strangles)), staphylococcus spp, arcanobacterium pyogenes, E. coli, klebsiella, pseudomonas)

junction between grey and white matter

may rupture/penetrate ventricular wall –> ventriculitis/ventricular abscess

chronic inflammatory process

37
Q

what is thrombotic meningoencephalitis (TME) of cattle

A

histophilus somni

commensal of resp system

bacteraemia

adherance to endothelial cells –> vasculitis, hemorrhage and local thrombosis

38
Q

what is arthropod-borne encephalitides

A

arboviruses (west nile virus, EEE, WEE, VEE, japanese encephalitis, louping ill)

neurotropic

polioencephalomyelitis

distribution varies according to agent:

west nile virus encephalitis –> brainstem + spinal cord

equine encephalitis –> cerebral cortex (+/- spinal cord)

vasculitis and thrombosis possible

39
Q

what is feline infectious peritonitis virus (coronavirus)

A

development of disease determined by type and degree of immunity (wet and dry form)

causes pyogranulomatous inflammation

surface associated –> meninges, periventricular white matter, eye (uvea, retina, optic nerve)

possible development of obstructive hydrocephalus

40
Q

what is hematogenous and leukocyte trafficking fungi

A

aspergillus spp, cryptococcus neoformans, blastomyces dermatitides, histoplasma capsulatum, coccidiodes immitis

usually opportunistic (immunocompromised)

gross: yellow-brown foci
histo: pyo granulomatous inflammation

41
Q

what is canine distemper

A

morbillivirus

pantropic, but particular affinity for lymphoid, epithelial and CNS tissue

in CNS: primary demyelinating; leukencephalomyelitis; ICBs

reaches CNS in secondary viremia; trafficking cells from perivascular cuffs –> spread to CNS in oligodendrocytes incomplete infection

42
Q

what is listeriosis

A

listeria monocytogenes

ruminants

silage

oral cavity –> cranial nerves (sensory + motor) –> midbrain and medulla oblongata; then bacterium spreads from cell to cell

injury is secondary to inflammation

histology: microabscesses and lymphoplasmacytic meningoencephalitis

43
Q

what is rabies

A

retrograde axonal transport virus

neurotropic visuses

infects nervous and non-nervous tissues (salivary glands)

gross: absent
histo: mononuclear polioencephalomyelitis (and meningitis)

negri bodies

44
Q

what is encephalitic herpesviruses (alpha-herpesviruses)

EHV-1, BHV-1/5, SHV-1 (pseudorabies)

neurotropic

A
45
Q

how does cell injury occur in encephalitic herpesvirus

A
  1. necrosis of infected neurons in glial cells
  2. necrosis of infected endothelial cells (EHV-1)
  3. secondary effects of inflammation
46
Q

what are the effects of encephalitic herpesviruses

A

leukocyte trafficking

latency in neural tissue

histology: neuronal degeneration and polioencephalomalacia; neuronal nuclear ICBs

47
Q

what is autoimmune encephalopathies

A

dogs

autoimmune etiology suspected

predisposed/overrepresented breeds

48
Q

what are the main forms of autoimmune encephalopathies

A
  1. meningoencephalitis of unknown origin (MUO): necorotizing or granulomatous (GME, NME, NLE)
  2. steroid-responsive meningitis-arteritis
  3. eosinophilic meningoencephalitis
49
Q

what are extrinsic spinal cord injuries

A
  1. RTA
  2. kicks
  3. crushing
  4. penetrating objects
50
Q

what are intrinsic traumas to spinal cord

A
  1. disc herniation
  2. spinal malformation
  3. pathological fractures
  4. absess
  5. neoplasia
51
Q

what is invertebral disc disease

A

common in dogs

degenerative changes in invertebral disk

herniations

T10-L3 > cervical

52
Q

what makes chondrodystrophic dogs susceptible to invertebral disc disease

A

premature degeneration

loss of notochordal cells mineralization of nucleus pulposus

degeneration of annulus fibrosis –> extrusion (hansen type 1)

53
Q

what is the type of disc disease common in non-chondrodystrophic dogs

A

aging change

atrophy of disc

weaking of annulus fibrosis –> hansen type II

54
Q

what is explosive disc disease

A

traumatic rupture of annulus fibrosis

intensive exercise

55
Q

what is wobbler syndrome

A

cervical stenotic myelopathy

horses, dogs (large breeds)

static or dynamic

genetic, dietary, congenital abnormalities

56
Q

what is wobblers in horses

A

static C5-C7 (1-4 y)

dynamic C3-C5 (8-18 m)

57
Q

what vertebral does wobblers affect in dogs typically

A

C5-7 (approx 1 y)

58
Q

what is cerebrocortical necrosis (CCN)

A

polioencephalomalacia

small and large animals

causes: thiamine deficiency, sulfure intoxication, lead, salt intoxication/water deprivation, hypoglycemia, cyanide intoxication

59
Q

what is tetanus

A

clostridium tetani

penetrating wound

retrograde transport to CNS

60
Q

at occurs when tetanus enters the CNS

A

transferred accross synapses –> binds to presynaptic inhibitory interneuron –> blocks release of inhibitory neurotransmitters (glycine, GABA) –> generalized spasms

61
Q

what are primary neoplasias

A

oligodendroglioma

astrocytoma

medulloblastoma

choroid plexus tumour

ependymoma

hemangiosarcoma

meningioma

62
Q

what are the 4 routes of infection

A
  1. direct extension
  2. hematogenous
  3. leukocyte trafficking
  4. retrograde axonal transport

Module 8 (43 decks)

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