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Module 8 > Tissue Injury + Repair 1 > Flashcards

Tissue Injury + Repair 1 Flashcards

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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
what are vascular insults to CNS
1. hemorrhage (focal) 2. ischemia
26
what are examples of hemorrhagic damages
1. spontaneous 2. hemorrhagic infarct 3. vascular rupture (trauma) 4. neoplastic origin
27
what are ischemic insults
fibrocartilagenous emboli common in dogs clinically: peracute, often lateralized spinal cord signs with no pain material thought to originate from nucleus puposus
28
what is meningitis
inflammation of meninges
29
what is encephalitis
inflammation of brain (leukencephalitis = white matter, polioencephalitis = grey matter)
30
what is myelitis
inflammation of spinal cord
31
what are the types of inflammation
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
what are the portals of entry of inflammation infections
1. direct extension 2. hematogenous 3. leukocyte trafficking 4. retrograde axonal transport
33
what occurs when a pathogen enters the brain
1. inflammation 2. disruption of BBB (hemorrhage and edema in addition)
34
what is direct extension entry of a pathogen
penetrating injury extension of nasal cavity/sinus infection via cribriform plate extension of middle or inner ear infection extension of osteomyelitis
35
what is suppurative meningitis and ventriculitis
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
what are brain abscesses
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
what is thrombotic meningoencephalitis (TME) of cattle
histophilus somni commensal of resp system bacteraemia adherance to endothelial cells --\> vasculitis, hemorrhage and local thrombosis
38
what is arthropod-borne encephalitides
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
what is feline infectious peritonitis virus (coronavirus)
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
what is hematogenous and leukocyte trafficking fungi
aspergillus spp, **cryptococcus neoformans,** blastomyces dermatitides, histoplasma capsulatum, coccidiodes immitis usually opportunistic (immunocompromised) gross: yellow-brown foci histo: pyo granulomatous inflammation
41
what is canine distemper
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
what is listeriosis
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
what is rabies
retrograde axonal transport virus neurotropic visuses infects nervous and non-nervous tissues (salivary glands) gross: absent histo: mononuclear polioencephalomyelitis (and meningitis) negri bodies
44
what is encephalitic herpesviruses (alpha-herpesviruses) EHV-1, BHV-1/5, SHV-1 (pseudorabies) neurotropic
45
how does cell injury occur in encephalitic herpesvirus
1. necrosis of infected neurons in glial cells 2. necrosis of infected endothelial cells (EHV-1) 3. secondary effects of inflammation
46
what are the effects of encephalitic herpesviruses
leukocyte trafficking latency in neural tissue histology: neuronal degeneration and polioencephalomalacia; neuronal nuclear ICBs
47
what is autoimmune encephalopathies
dogs autoimmune etiology suspected predisposed/overrepresented breeds
48
what are the main forms of autoimmune encephalopathies
1. meningoencephalitis of unknown origin (MUO): necorotizing or granulomatous (GME, NME, NLE) 2. steroid-responsive meningitis-arteritis 3. eosinophilic meningoencephalitis
49
what are extrinsic spinal cord injuries
1. RTA 2. kicks 3. crushing 4. penetrating objects
50
what are intrinsic traumas to spinal cord
1. disc herniation 2. spinal malformation 3. pathological fractures 4. absess 5. neoplasia
51
what is invertebral disc disease
common in dogs degenerative changes in invertebral disk herniations T10-L3 \> cervical
52
what makes chondrodystrophic dogs susceptible to invertebral disc disease
premature degeneration loss of notochordal cells mineralization of nucleus pulposus degeneration of annulus fibrosis --\> extrusion (hansen type 1)
53
what is the type of disc disease common in non-chondrodystrophic dogs
aging change atrophy of disc weaking of annulus fibrosis --\> hansen type II
54
what is explosive disc disease
traumatic rupture of annulus fibrosis intensive exercise
55
what is wobbler syndrome
cervical stenotic myelopathy horses, dogs (large breeds) static or dynamic genetic, dietary, congenital abnormalities
56
what is wobblers in horses
static C5-C7 (1-4 y) dynamic C3-C5 (8-18 m)
57
what vertebral does wobblers affect in dogs typically
C5-7 (approx 1 y)
58
what is cerebrocortical necrosis (CCN)
polioencephalomalacia small and large animals causes: thiamine deficiency, sulfure intoxication, lead, salt intoxication/water deprivation, hypoglycemia, cyanide intoxication
59
what is tetanus
clostridium tetani penetrating wound retrograde transport to CNS
60
at occurs when tetanus enters the CNS
transferred accross synapses --\> binds to presynaptic inhibitory interneuron --\> blocks release of inhibitory neurotransmitters (glycine, GABA) --\> generalized spasms
61
what are primary neoplasias
oligodendroglioma astrocytoma medulloblastoma choroid plexus tumour ependymoma hemangiosarcoma meningioma
62
what are the 4 routes of infection
1. direct extension 2. hematogenous 3. leukocyte trafficking 4. retrograde axonal transport

Module 8 (43 decks)

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