Tissue Injury + Repair 1 Flashcards
what are the functions of neurons (3)
- transmission of impulses
- spatial and temporal interpretation of impulses
- 1inhibitory and stimulatory regulation of impulses
what are the function of astroglia
- regulation of extracellular neurotransmitter concentration
- fluid/electrolyte imbalances
- repair of injury (proliferation of processes)
- bundling of axons
- part of barrier system (glia limitans, BBB)
what is the function of oligodendroglia
myelination of axons in CNS
possible neuronal body homeostasis
what are the function of ependymal cells
movement of CSF through ventricular system
what is the function of the choroid plexus
secretion of CSF, barrier function (B-CSF-B)
what are the functions of microglia
immunosurveillance
immunoregulation
phagocytosis
what are the functions of the meningeal cells
barrier function (arachnoid-CSF-B)
subarachnoid CSF cushions brain
what are the functions of the endothelial cells
barrier function (BBB)
selective molecule tranport system
what are the cells involved with tissue injury and repair
- atroglia: repair of injury, part of barrier system (glia limitans, BBB)
- choroid plexus epithelial cells: barrier function (B-CSF-B)
- meningeal cells: barrier function (arachnoid-CSF-B)
- endothelial cells: barrier function BBB
what are the general concepts for understanding CNS injury (7)
- cells of CNS vary in susceptibility to injury: neurons –> oligodendrocytes –> astrocytes –> microglia –> blood vessels
- regeneration of neurons
- no or only very little regeneration of nerve fibres in CNS (better in PNS)
- 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)
- 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
- CNS has fair ability to resist infection and injury. Once infected low degree of resistance compared to other tissues
what are the defence mechanisms of the CNS
- skin
- bony structures (calvarium/vertebrae)
- meninges, CSF
- barrier systems: BBB, B-CSF-B, glia limitans, arachnoid-CSF-B
- local innate immune system: microglia and astrocytes
- trafficking macrophages
- innate and adaptive immune system once BBB broken down
what is the neuron response to CNS tissue injury
- ischemic change (necrotic cell death) –> ischemia, bacterial toxins, inflammatory mediators, thermal injury, heavy metals, nutritional deficiencies (thiamine), trauma, ATP production decreased
- inclusion body formation
- cytoplasmic vacuolation (spongiform encephalopathy)
- central chromatolysis (dispersion of nissl substance –> axonal injury)
- intracytoplasmic deposition of material (storage disease, aging)
what are the responses of astrocytes to tissue injury
- swelling, hypertrophy, division, increased processes
- astrocytosis (increase in size + #)
- astrogliosis (hypertrophy –> more processes, ect. gemistocytes)
- formation of glial scar
what are oligodendrocytes response to tissue injury
- swelling, hypertrophy, degeneration (only precursors proliferate)
- satellitosis
- degeneration due to ischemia, viruses, lead, autoimmunity –> (primary) demyelination
- axonal injury leads to secondary demyelination
what are the ependymal and choroid plexus cells
- atrophy (ex. hydrocephalus), degeneration, necrosis
- no regeneration, instead astrogliosis
what are the responses of microglia to injury
- hypertrophy
- hyperplasia (glial nodules together with other cells)
- phagocytosis
- neuronophagia
what are the responses of meninges to injury
inflammatory changes (meningitis)
proliferation
mineralization
what are gitter cells
tissue necorsis
macrophages derived from blood monocytes
phagocytose lipid-laden debris –> foamy
what are the damages that can injure the CNS
- necrosis (any cell type)
- inflammation
- vascular changes (edema, swelling)
- gliosis –> proliferation of astrocytes, oligodendrocytes, microglia
- fibrosis (not really only astrocyte proliferation)
- severe inflammation –> severe tissue damage/necrosis (encephalomalacia)
- inflammation of CSF compartment –> obstruction of CSF flow –> hydrocephalus
- specific to axonal injury: Wallerian degeneration, central chromatolysis
- demyelination: primary and secondary
what is Wallerian degeneration
degeneration of axon (and dendritic processes) independently of neuronal cell body; CNS and PNS
what is the process of wallerian degeneration
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)
how does regeneration occur in the PNS with wallerian degeneration
formation of Bungner’s bands
axonal sprouting
segmental remyelination
what is the result of wallerian degeneration in the CNS
axonal loss and reactive astrogliosis (scar)
what are the damage to CNS
- vascular
- inflammatory (infection/immune-mediated)
- traumatic
- anomaly
- metabolic toxic
- iatrogenic/idiopathic
- neoplastic
- degenerative
what are vascular insults to CNS
- hemorrhage (focal)
- ischemia
what are examples of hemorrhagic damages
- spontaneous
- hemorrhagic infarct
- vascular rupture (trauma)
- neoplastic origin
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
what is meningitis
inflammation of meninges
what is encephalitis
inflammation of brain
(leukencephalitis = white matter, polioencephalitis = grey matter)
what is myelitis
inflammation of spinal cord
what are the types of inflammation
- suppurative: bacteria
- lymphocytic and histiocytic: viruses, protozoa
- granulomatous: fungi, protozoa, higher order bacteria (mycobacterium spp)
- eosinophilic: parasitic larval migration (salt poisoning in pigs)
what are the portals of entry of inflammation infections
- direct extension
- hematogenous
- leukocyte trafficking
- retrograde axonal transport
what occurs when a pathogen enters the brain
- inflammation
- disruption of BBB (hemorrhage and edema in addition)
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
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
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
what is thrombotic meningoencephalitis (TME) of cattle
histophilus somni
commensal of resp system
bacteraemia
adherance to endothelial cells –> vasculitis, hemorrhage and local thrombosis
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
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
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
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
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
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
what is encephalitic herpesviruses (alpha-herpesviruses)
EHV-1, BHV-1/5, SHV-1 (pseudorabies)
neurotropic
how does cell injury occur in encephalitic herpesvirus
- necrosis of infected neurons in glial cells
- necrosis of infected endothelial cells (EHV-1)
- secondary effects of inflammation
what are the effects of encephalitic herpesviruses
leukocyte trafficking
latency in neural tissue
histology: neuronal degeneration and polioencephalomalacia; neuronal nuclear ICBs
what is autoimmune encephalopathies
dogs
autoimmune etiology suspected
predisposed/overrepresented breeds
what are the main forms of autoimmune encephalopathies
- meningoencephalitis of unknown origin (MUO): necorotizing or granulomatous (GME, NME, NLE)
- steroid-responsive meningitis-arteritis
- eosinophilic meningoencephalitis
what are extrinsic spinal cord injuries
- RTA
- kicks
- crushing
- penetrating objects
what are intrinsic traumas to spinal cord
- disc herniation
- spinal malformation
- pathological fractures
- absess
- neoplasia
what is invertebral disc disease
common in dogs
degenerative changes in invertebral disk
herniations
T10-L3 > cervical
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)
what is the type of disc disease common in non-chondrodystrophic dogs
aging change
atrophy of disc
weaking of annulus fibrosis –> hansen type II
what is explosive disc disease
traumatic rupture of annulus fibrosis
intensive exercise
what is wobbler syndrome
cervical stenotic myelopathy
horses, dogs (large breeds)
static or dynamic
genetic, dietary, congenital abnormalities
what is wobblers in horses
static C5-C7 (1-4 y)
dynamic C3-C5 (8-18 m)
what vertebral does wobblers affect in dogs typically
C5-7 (approx 1 y)
what is cerebrocortical necrosis (CCN)
polioencephalomalacia
small and large animals
causes: thiamine deficiency, sulfure intoxication, lead, salt intoxication/water deprivation, hypoglycemia, cyanide intoxication
what is tetanus
clostridium tetani
penetrating wound
retrograde transport to CNS
at occurs when tetanus enters the CNS
transferred accross synapses –> binds to presynaptic inhibitory interneuron –> blocks release of inhibitory neurotransmitters (glycine, GABA) –> generalized spasms
what are primary neoplasias
oligodendroglioma
astrocytoma
medulloblastoma
choroid plexus tumour
ependymoma
hemangiosarcoma
meningioma
what are the 4 routes of infection
- direct extension
- hematogenous
- leukocyte trafficking
- retrograde axonal transport
