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84 Cards in this Set

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Pathogenesis of Congenital Hydrocephalus.
occlusion of CSF flow, usu. Cerebral aqueduct (it's narrow).
Pathogenesis of Acquired Hydrocephalus.
occlusion of CSF flow, usu. Cerebral aqueduct (it's narrow).
Pathogenesis of Congential Hydromyelia.
occlusion of CSF flow in central canal.
Pathogenesis of Acquired Hydromyelia.
occlusion of CSF flow in central canal.
Pathogenesis of Syringomyelia.
unrelated to CSF flow, ventricular system or central canal.
Pathogenesis of Hydrancephaly.
infarct.
Pathogenesis of Meningoencephalocele.
failure of neural tube to close, and failure of sutures to close.
Pathogenesis of Meningomyelocele.
failure of neural tube to close, and failure of vertebral arches to close.
Pathogenesis of Supparative Meningitis.
pia-arachnoid layer (leptomeninges).
Pathogenesis of Neonatal Bacterial Meningitis.
microbial entry via umbilicus, hemotogenous spread and replication, bacterial emboli get trapped in meninges.
Pathogenesis of Adult Bacterial Meningitis.
microbial entry via castration, ear notching wound, hemotogenous spread and replication, bacterial emboli get trapped in meninges.
Pathogenesis of Rabies.
peripheral nerves--replication in monocytes-->retrograde neuronal transport--> replication in CNS, --> anteriograde neuronal transport--> salivary gland and replication in epithelia cells --> out via saliva.
Pathogenesis of Brain Abscesses.
entry and replication of microbe in wound-->hematogenous spread, or direct extension from inner ear of cribiform plate.
Pathogenesis of Spinal Cord Abscesses.
bacterial emboli lodge in bone--pinch off --pinch off spinal cord.
Pathogenesis of Protozoal encephalomyelitis.
leukocytes trafficking--spread via monocytes, infection of endothelial cells -->granulomatous vascultis-->infarct--> hypoxia--> necrosis.
Pathogenesis of Fungal encephalomyelitis.
inhaled (blasts/histo) or skin wound --> hematogenous spread to CNS via monocyte trafficking, OR direct extension from nasal sinuses through cribiform plate (usu crypto).
Pathogenesis of Cryptococcal Encephalomyelitis.
From the Sinuses and cribriform plate into the meninges and brain .
Pathogenesis of Myelin Storage Disease.
macrophage cannot digest fat, other macrophages move in, buildup of macrophages, unprocessed lipid buildup, pschosine toxic effect on oilgodendroglial cells.
Pathogenesis of Congential Hepatic Encephalopathy.
toxins pass liver and get to CNS, causing elevate ammonia, and other protein metabolites--> alteration in ATPase dependent Na/K pumps-->electrolyte imbalance and fluid shift--> edema--> increased ICP.
Pathogenesis of Acquired Congential Hepatic Encephalopathy.
toxins pass liver and get to CNS, causing elevate ammonia, and other protein metabolites--> alteration in ATPase dependent Na/K pumps-->electrolyte imbalance and fluid shift--> edema--> increased ICP.
Pathogenesis of Renal Encephalopathy (aka Uremic Encephalopathy).
toxins pass liver and get to CNS, causing elevate ammonia, and other protein metabolites--> alteration in ATPase dependent Na/K pumps-->electrolyte imbalance and fluid shift--> edema--> increased ICP.
Pathogenesis of Cytotoxic Cerebral Edema.
ischemia-->altered cellular metabolism, IC accumulation of fluid in neurons and glial cells--direct cellular damage--> death.
Pathogenesis of Vasogenic Cerebral Edema.
vascular injury with extravascular accumulation of fluid, breakdown of BBB.
Pathogenesis of Hydrostatic Cerebral Edema.
elevated ventricular hydrostatic pressure (i.e. hydrocephalus) EC accumulation of fluid.
Pathogenesis of Osmotic Cerebral Edema.
osmotic imbalance, EC fluid accumulation in grey, white matter.
Pathogenesis of Brain swelling.
like edema, causes increased ICP--> death.
Pathogenesis of Increased ICP.
from 1) brain swelling or 2) edema, 3) space occupying mass or 4) inflammation.
Pathogenesis of Cerebellar (Cortical) Abiotrophy.
intrinsic metabolic defect that causes premature death of neurons, degeneration of cells after normal development.
Pathogenesis of Trauma due to CNS Coup-Contrecoup.
coup at site of impact, contrecoup result of brain banging around inside cranium--Opposite site of impact.
Pathogenesis of Trauma due to Diffuse Axonal Shearing.
distortion of brain, collision of brain with skull, axon stretched and torn, shearing effects.
Pathogenesis of Aneurysm.
weakness in wall of vessel--localized abnormal dilation of blood vessel.
Pathogenesis of Transectional Axonopathies.
transection of axon-->axonal damage, collapse of endoneurial tube, phagocytosis of axonal debris, proliferation of replacement tissue (oligodendroglial cells--brain or Schwann cells--cord).
Pathogenesis of Stenotic Cervical Myelopathy.
bone problem--canal is small.
Pathogenesis of Intervertebral Disc Disease.
bulging or extruded disc material puts pressure on spinal cord.
Pathogenesis of Vertebral Malformations.
in utero anomaly.
Pathogenesis of Fibrous Astrocytoma.
proliferation of malignant astrocytes.
Pathogenesis of Canine Distemper.
CNS disease is secondary condition of CDV infection; aerosol transmission, microbe trapped in mucosa of nasal turbinates, replication in macrophages and neutrophils, leukocytic trafficking to local lymph nodes (retropharyngeal)), more replication in lymph nodes, 1° viremia of systemic lymph nodes, spleen, thymus, immunosuppression, 2° viremia (via leukocyte trafficking) infects CNS as well as epithelial cells all through body .
Pathogenesis of Canine Distemper--Acute phase.
CNS disease is secondary condition of CDV infection; aerosol transmission, microbe trapped in mucosa of nasal turbinates, replication in macrophages and neutrophils, leukocytic trafficking to local lymph nodes (retropharyngeal)), more replication in lymph nodes, 1° viremia of systemic lymph nodes, spleen, thymus, immunosuppression, 2° viremia (via leukocyte trafficking) infects CNS as well as epithelial cells all through body .
Pathogenesis of Canine Distemper--Demyelinating phase.
previous infection with CDV .
Pathogenesis of Chronic CDV Encephalitis (aka old dog encephalitis).
autoimmune response to neuronal tissue--expansile process-->compression of adjacent tissue-->compressive axonopathy lesion like Wallerian degeneration.
Pathogenesis of Granulomatous meningoencephalitis.
proliferative response of monocytes derived from bone marrow, aberrant host response or true neoplastic disease.
Pathogenesis of Inflammatory reticulosis.
Proliferative response of mononuclear phagocytes (monocytes) derived from bone marrow, Aberrant host response, True neoplastic disease (Markers for neoplastic lymphocytes have been demonstrated in these foci).
Pathogenesis of Neoplastic Reticulosis.
Proliferative response of mononuclear phagocytes (monocytes) derived from bone marrow, Aberrant host response, True neoplastic disease (Markers for neoplastic lymphocytes have been demonstrated in these foci).
Pathogenesis of Neuropododermatitis.
loss of sensation--> mutilation or injury .
Pathogenesis of Idiopathic Polyradiculoneuritis.
Raccoon bite associated, Similar to Guillain-Barre syndrome, May be a postinfectious phenomenon, Postvaccinal or Postinfectious-immune mediated disease.
Pathogenesis of Congential Myasthenia Gravis.
reduce # of ACh receptors in postsynaptic membrane of myoneural jx, fewer impulses from synapse -->muscle weakness.
Pathogenesis of Acquired Myasthenia Gravis.
HST II, seen with thymitis and thymoma, induced by T-lymphocytes that recognize myocytes with ACh receptor in thymus (wow! we're actually applying immuno!), cross-reacting Ab's go systemic to attack myocytes.
Pathogenesis of Dural Ossification.
metaplasia due to dural irritation.
Pathogenesis of Cerebrovascular Atherosclerosis.
metabolic vascular injury--> abnormal lipid deposition in intima and media of arteries.
Pathogenesis of Brain-Heart Syndrome.
over stimulation of beta-receptors, which are abundant in heart.
Pathogenesis of Degenerative Myelopathy in dogs.
UNKNOWN--besides axonal degeneration, secondary Wallerian demyelination.
Pathogenesis of Degenerative Myelopathy in cats.
UNKNOWN--besides axonal degeneration, secondary Wallerian demyelination.
Pathogenesis of Dysautonomia.
PNS disease--enteric division.
Pathogenesis of Viral Cerebellar Hypoplasia.
in utero infection, transplacental hematogenous infection, breach of BBB-->virus gets in, affect external germinal layer of cerebellum, cytolysis by virus, no internal granular layer formed, so other layers don’t form.
Pathogenesis of Genetic Cerebellar Hypoplasia.
mutation of cells that affect differentiation, migration of cells in embryo-->atophy or hypoplasia.
Pathogenesis of Feline Infectious Peritonitis.
HST III.
Pathogenesis of Feline Ischemic Encephalopathy.
infarct, vasculitis, altered vasc, flow from thrombosis and infarct from larval parasite--Cuterebra spp. .
Pathogenesis of Protozoal Encephalomyelitis.
ingested in filed, food, passed by skunks, possums feces, phagocytized by macrophages.
Pathogenesis of acute/sudden Protozoal Encephalomyelitis.
inflammation, thrombosis.
Pathogenesis of progressive/slow Protozoal Encephalomyelitis.
encysted parasite.
Pathogenesis of Herpes Virus Encephalitis.
Hematogenous spread (viremia; also in leukocytes), Virus infects endothelial cells, Thrombosis of small arteries and veins, Virus induced ischemic vasculitis.
Pathogenesis of Arboviral Encephalomyelitis .
mosquito vectors, bird reservoirs, hematogenous spread.
Pathogenesis of West Nile Virus.
mosquito vectors, bird reservoirs, hematogenous spread.
Pathogenesis of Leukoencehaphalo malacia .
unknown--targeted toxin, mechanism unknown.
Pathogenesis of Cerebrospinal Nematodiasis.
Fourth stage larvae migrate in vessel walls, Thrombosis/thromboembolism, Parasite and platelet/fibrin embolus lodge in brain, Parasites migrate out of vessel into neuropil.
Pathogenesis of Laryngeal Hemiplegia.
atrophy/paralysis of left cricoaritenoideus dorsalis mm.
Pathogenesis of Botulism.
spores release toxin to necrotic tissue, carry via blood to systemic circ.--Blocks Ach release.
Pathogenesis of Toxicoinfections Botulism in foals.
from nibbling at dirt.
Pathogenesis of Tetanus.
inhibits inhibitory neurons.
Pathogenesis of Cauda Equina Neuritis.
loss of myelin and neuronal degeneration.
Pathogenesis of Dummy Foal Syndrome .
restricted cerebral perfusion at birth--twisted umbilicus, compression of blood supply.
Pathogenesis of Equine Lower Motor Disease.
free rads case lipid membrane damage to neurons.
Pathogenesis of Listeriosis: brain stem of cow gives it away.
sores from foreign body penetration of mucosa in mouth, esoph, organism follows cranial nerves into brain stem enzymes released from neutrophils early on ---retrograde axonal transport.
Pathogenesis of Thrombic Meningiencephalitis.
infarcts from vasculitis.
Pathogenesis of Polioencephalitis.
altered metabolic energy pd'n of neurons, mitochondrial generation of ATP/use of O2.
Pathogenesis of Lead encephalopathy.
lead breached BBB, vasogenic edema, laminar cortical necrosis.
Pathogenesis of Symmetrical Encephalomalacia.
Rapid replication of C. perfringens, Exotoxin produced in intestinal tract, Exotoxin absorbed by intestine, Hematogenously spread to certain brain stem nuclei that have a selective vulnerability for the toxin.
Pathogenesis of Spongiform Polioencephalopathy.
Progressive neuronal degeneration, Abnormal forms of prion protein.
Pathogenesis of Lentivirus Encephalitis.
Milk and respiratory secretions, Macrophage leukocytic trafficking, Persistent infection, mmune mediated disease.
Pathogenesis of Viral Leuko-encephalomyelitis.
Milk and respiratory secretions, Macrophage leukocytic trafficking, Persistent infection in neural cells, Immune mediated disease, Lesions also in brain.
Pathogenesis of Caprine Arthritis Encephalitis.
Milk and respiratory secretions, Macrophage leukocytic trafficking, Persistent infection in neural cells, Immune mediated disease, Lesions also in brain.
Pathogenesis of Pseudorabies.
Neuronal entry (sensory nerve endings), Retrograde axonal transport to brain (Trigeminal nerve and ganglion, Olfactory nerve), Neural cell degeneration and necrosis.
Pathogenesis of Eosinophilic Meningoencephalitis.
Hypernatremic syndrome, Movement of water back and forth across osmotic barriers in relationship to osmotic gradients, Inhibition of glycolysis in neurons and/or damage to blood-brain barrier with edema (vasogenic).
Pathogenesis of Cerebrospinal Angiopathy.
Edema disease principle (EDP), Gram negative bacterial endotoxin that is neurotoxic, Acts at blood-brain barrier, Affects vascular endothelial function, Alters function of neurons.