Neuropath- Part 6

Card Set Information

Neuropath- Part 6
2015-10-22 14:38:47
neuropath vetmed

vetmed neuropath
Show Answers:

  1. FIP virus infection leads to _____________ damage; it is caused by a _________, resulting in ___________.
    host-mediated endothelial; coronavirus; multisystemic necrotizing vascular disease
  2. Cats are infected with coronavirus FIP at a(n) _______ age; persistent low level viral antigen expression results in ___________.
    young;high antiviral antibody titer
  3. When persistent FIP virus is reactivated or the cat is infected with a related coronavirus, there is __________ formation and deposition in vessels, resulting in _________; the __(2)__ are the organs most commonly affected.
    immune complex; vasculitis; kidney and retina
  4. Describe the acute necrotizing form of FIP.
    vascular effusion- "wet form"
  5. Describe the subacute/inflammatory form of FIP.
    multifocal pyogranulomatous inflammation of vessels- "dry form"
  6. CNS involvement of FIP leads to __________ and _________ exudation into the ________.
    hydrocephalus; fibrinous; CSF
  7. Hematogenous dissemination of fungal yeast results in seeding of the ____________; systemic mycoses include... (4)
    leptomeninges; Histoplasma, Blastomyces, Coccidioides, Cryptococcus
  8. The most frequently encountered CNS mycosis.
    Cryptococcus neoformans
  9. Entry of Cryptococcus can be by... (2)
    hematogenous or by direct extension from nasal cavity
  10. Pathogenic variants of Cryptococcus have a __________ that resists phagocytosis, so that _________ is minimal; CNS lesions are __________ with a ________ inflammatory response.
    thick mucopolysaccharide capsule; inflammation; solid masses of organisms; minimal
  11. Opportunistic fungi cause __(2)__ because hyphae invade __________ when the immune system is suppressed; opportunistic fungi include... (4)
    vasculitis and thrombosis; endothelial cells; Aspergillus, Mucor, Rhizopus, Candida
  12. Describe the life cycle of Phylum Apicomplexa.
    intestinal infection of DH and sexual replication with shedding of oocysts; asexual replication in endothelium of IH, encystment in IH
  13. Apicomplexa protozoa have a predilection for CNS invasion in ___________.
    atypical IH
  14. Toxoplasma gondii: DH, IH, atypical IH
    • DH: cat
    • IH: rodent
    • atypical: cats, other carnivores/omnivores
  15. Neosporum caninum: DH, IH, atypical IH
    • DH: dog
    • IH: cattle
    • atypical IH: dog
  16. Sarcocystic neurona: DH, IH, atypical IH
    • DH: opposum
    • IH: raccoon
    • atypical IH: horse, dog
  17. Equine protozoal myeloencephalitis is caused by infection with __________; lesion development is associated with ____________ in the __________.
    Sarcocystis neurona; asexual replication; IH
  18. Horses are infected with Sarcocystis by ________; sporozoites are released in the _________; viral replication takes place in __(2)__ and _________ occurs.
    ingestion; intestine; vessels and muscle; encystment
  19. With EPM, Sarcocystis has tropism for __________, targeting the organism to the __(2)__.
    certain vascular beds; brainstem and spinal cord
  20. Unlike herpesvirus infection, sarcocystis gross lesions are...
    distributed b/w grey and white matter; there are perivascular cuffs of inflammatory cells
  21. Parasitic or verminous encephalomyelitis is caused by ____________, which undergo __________ in the __________ OR by CNS migration in a(n) ___________.
    metazoan (multicellular); aberrent migration; normal DH; aberrent host
  22. Immune-mediated process in which the antigenic target is a CNS antigen or CNS tissue is damaged in a by-stander fashion.
  23. Repetitive episodes that promote high level lymphocyte trafficking in the CNS plus undesirable Ag presentation.
    allergic encephalitis
  24. Infectious agents are often incriminated in allergic encephalitis because... (3)
    cause increased leukocyte trafficking in CNS, inflammatory cytokines induce MHC, molecular mimcry
  25. Cauda equine neuritis is _____________; there is ___(2)___ of the extradural portion of the caudal equina, leading to __(2)__.
    autoimmune radiculoneuritis; granulomatous and lymphoplasmacytic inflammation; demyelination and axonal degeneration
  26. Disorder in which antibody directed against the motor end plate results in periodic weakness (associated with exercise) that is not associated with histological changes.
    Myasthenia gravis
  27. Expansile perivascular accumulation of cells in the central nervous system.
  28. Granulomatous meningoencephalitis is _____________; and the two types are __(2)__.
    idiopathic reticulosis; neoplastic and inflammatory
  29. What are the histological and gross characteristics of inflammatory idiopathic reticulosis?
    pleomorphic pop of lymphocytes, histiocytes, and plasma cells; disseminated throughout WM of CNS, focal in WM of CNS, or involvement of optic nerves
  30. What are the histological and gross characteristics of neoplastic idiopathic reticulosis?
    isomorphic cell population, perivascular foci that tend to coalesce; single masses grossly
  31. Necrotizing meningoencephalitis involves __(3)__; there are ___________ infiltrates, and __________ is pronounced.
    cortical leptomeninges, grey matter, and white matter; inflammatory; necrosis
  32. What lesions are characteristic of degenerative disorders? (3)
    non-inflammatory, selective, symmetrical
  33. What is the scrapies prion protein derived from?
    cellular membrane protein that is abundantly expressed on neurons and lymphocytes
  34. How is scrapies prion protein derived from a normal cell membrane protein?
    PrPc is periodically internalized, unfolded, and refolded; mal-folding can lead to production of PrPsc
  35. How is PrPsc acquired? (2)
    mal-folding of PrPc can occur spontaneously, it can be acquired through ingestion of PrPsc in meat or milk (causing further mal-folding of PrPc)
  36. The initial conversion of PrPc to PrPsc likely occurs in _________, which is __________; this accounts for transmission to the NS.
    gut-associated lymphoid tissue; innervated
  37. Why is PrPsc a problem?
    PrPc provides an important antioxidant function; its loss predisposes neurons to oxidative injury
  38. Lesions associated with prion infections.
    neuronal vacuolation within brainstem nuclei, most pronounced within the reticular formation, dorsal nucleus of the vagus nerve, and lateral cuneate nucleus
  39. A neuraxonal dystrophy affecting proprioceptive system neurons, manifesting as spinal cord disease.
    degenerative myeoencephalopathy
  40. With degenerative myeloencephalopathy, the functional defect involves ___________ axoplasmic transport; presentation is often _____________.
    slow antegrade; progressive ataxia
  41. Spheroids in proximal axon segments, containing neurofilament tangles, membranous whorls, and lysosomal bodies are anatomic changes associated with _____________.
    degenerative myeloencephalopathy
  42. Changes associated with degenerative myeloencephalopathy are most dramatic in the __________ nuclei in the brainstem at the level of the ________.
    proprioceptive; obex
  43. A progressive, age-related degeneration of myelinated axons that is also thought to represent an axoplasmic transporter defect; heritable defect in superoxide dismutase.
    degenerative myelopathy of old dogs
  44. Axon cylinder swelling and fragmentation associated with old dog degenerative myelopathy is most consistent with a defect in ___________.
    fast antegrade transport
  45. Describe the distribution of lesions that occur with degenerative myelopathy of old dogs? What is a secondary lesion?
    diffuse in thoracic and cranial lumbar region of the spinal cord; secondary denervation atrophy of muscle
  46. Progressive neuronal degeneration reflecting metabolic defects of Purkinje cells and affected extrapyramidal neurons; multiple system degeneration.
    cerebellar abiotrophy
  47. Cerebellar abiotrophy is death of cell that had __________; it is most likely ________ origin in dogs.
    developed normally; heritable
  48. Heritable abiotrophies are associated with decreased numbers of _________, dysplastic ___________, and symmetrical degeneration of ____________.
    Purkinje cells; Purkinje cells; extrapyramidal nuclei (olivary, pontine,and basal nuclei)
  49. Acquired abiotrophy in cattle arises from ___________; __________ are destroyed, and signs a referrable to ____________.
    plant toxicity; Purkinje cells; cerebellar dysfunction
  50. Selective loss of LMN in the spinal cord that is characterized by progressive weakness and muscle wasting due to secondary denervation atrophy.
    LMN disease (commonly Equine LMN disease)
  51. The acquired nature of equine LMN disease is suggested by association with low blood levels of ____________ with a role of ________ in producing neuronal injury.
    Vitamin E; free radicals
  52. What pathologic change is acute intoxication with organophosphates associated with?
    no pathologic change- results in accumulation of Ach at synapses and motor end plates
  53. With a general insult, _________ are most susceptible; __________ are the second most susceptible.
    neurons; oligodendrocytes
  54. Metabolic/nutritional/toxic conditions that are characterized by selective necrosis WITHOUT malacia. (4)
    hypoglycemia, hypoxia/anoxia, neonatal maladjustment syndrome, hepatoencephalopathy
  55. How does hypoglycemia affect the brain?
    primary energy failure; neurons are affected first; occurs too quickly for signs of necrosis to develop
  56. What cells are most susceptible to death due to hypoglycemia?
    neurons in the superficial cerebral cortex and hippocampus
  57. Lack of oxygen compromises __________ and ultimately leads to cell death.
    oxidative metabolic pathways
  58. Causes of hypoxia. (4)
    cardiac disease, pulmonary disease, anemia, polycythemia
  59. Causes of anoxia. (2)
    anesthetic arrest followed by revival, seizure
  60. What is neonatal maladjustment syndrome?
    perinatal hypoxic/ischemic encephalopathy- low BP and low blood oxygen tension leading to selective neuronal necrosis
  61. Lack of portal blood processing can be caused by __(2)__; a characteristic but rare finding associated with heptoencephalopathy is...
    portal-caval shunt; primary liver disease; elevated blood ammonia, which leads to primary demyelination due to intramyelenic edema.
  62. What are the functional derangements of the liver that can lead to heptoencephalopathy? (3)
    impaired energy metabolism, exposure to false neurotransmitters (things that should be removed by the liver), toxicity associated with elevated blood ammonia
  63. Metabolic/nutritional/toxic conditions characterized by selective neuronal necrosis WITH malacia. (4)
    Thiamine deficiency, salt intoxication, focal symmetrical encephalomalacia (FSE), lead poisoning
  64. What is thiamine required for in the CNS?
    cofactor in oxidative energy pathways, deficiency results in decrease high-energy phosphate levels
  65. Thiamine deficiency is characterized by what CNS changes?
    vascular damage and neuronal necrosis progressing to malacia
  66. Rumenal microflora normall produce thiamine; deficiencies are encountered in... (3)
    decreased rumenal production (low rumen pH due to high concentrate diet), consumption of thiaminase containing plants, decreased thiamine bioavailability (high sulfur diet)
  67. Describe the progression of lesions in ruminants with thiamine deficiency.
    cerebral swelling +/-herniation --> ischemic necrosis of cerebrum--> live of cavitation b/w grey and white matter (autofluoresces)
  68. ___________ require dietary thiamine; deficiency results in... (2)
    Carnivores; hemorrhage, pannecrosis of periventricular nuclei
  69. Describe how salt intoxication causes neuronal necrosis.
    brain becomes hyperosmolar compared to plasma--> cytotoxic edema and brain swelling--> cortical ischemia--> neuronal necrosis and malacia
  70. Describe how a calf would become salt intoxicated.
    animal is hypernatremic due to increased sodium intake or water deprivation--> brain cells accumulate idiogenic osmoles--> animal gains access to fresh water--> brain cells require time to eliminate osmoles, therefore, they swell--> cerebral circulation is impeded by tissue expansion within cranial vault--> edema neuronal necrosis, malacia
  71. Focal symmetrical encephalomalacia is caused by..
    enteric overgrowth of C. perfringens type D or E. coli, absorption and systemic dissemination of their toxins, inducing widespread vascular damage, and triggering the edema cycle
  72. FSE triggers the __________ and the result is __________.
    edema cycle; polioencephalomalacia
  73. How do you distinguish polioencephalomalacia caused by bacterial exotoxin from that caused by thiamine deficiency or salt intoxication?
    with FSE, vascular damage may be apparent in other organs; lesions are observed in specific brain nuclei (basal nuclei, thalamus, substantia nigra w/ FSE)
  74. How does lead poisoning lead to malacia?
    lead binds to and damages vascular endothelium, resulting in edema and alteration of the BBB; also, toxic to neurons and schwann cells
  75. Malacia in white matter is either...
    pannecrosis or demyelination.
  76. Moldy corn poisoning leads to ___________ in _________.
    leukoencephalomalacia; horses
  77. Malacia associated with moldy corn poisoning is secondary to _____________ and sometimes __________.
    pronounced vasogenic edema; hemorrhage
  78. __(2)__ lesions tend to produce greater alterations in CSF than do ________ lesions.
    Meningeal and paraventricular; deeper parenchymal
  79. _________ diseases are more likely to have abnormal CSF than are _________ diseases.
    acute; chronic
  80. What are indications for CSF analysis? (3)
    abnormal neurologic exam, recurring fever of undetermined origin, neck/limb pain
  81. What are contraindications for CSF analysis, and how do you determine this?
    post-trauma or increased intracranial pressure; determined by decreasing level of consciousness, non-responsive pupils, rigid paresis, and altered respiratory patterns/cardiac rhythms
  82. What can happen if you sample CSF from a patient with increased intracranial pressure?
    brain herniation- usually fatal- most serious complication that can occur with CSF sampling
  83. What are the methods of CSF collection in which species? (3)
    atlantooccipital puncture (cerebromedullary cistern)- all, lumbar cisternal puncture- dogs, lumbosacral interspace-cats, LA
  84. How do you collect CSF for cytology? For culture?
    cytology- EDTA (normal CSF shouldn't clot, so serum tube may be adequate); culture- serum tube (EDTA is not sterile)
  85. If CSF analysis is delayed, store at ________ for a maximum of ________.
    4°C; 4-8hr
  86. What is the normal color and clarity of CSF?
    colorless and clear
  87. Pink to bright red CSF may indicate...
    traumatic tap, recent hemorrhage [centrifuge- becomes clear means iatrogenic blood or VERY recent hemorrhage, stays pink means hemorrhage at least 10hr ago]
  88. Dull red or brown CSF may indicate...
    hemorrhage 24-48hr ago
  89. Xanthochromia is _________ color due to release of ________; this occurs ___________.
    yellow-orange; bilirubin from engulfed RBCs; 12 hrs after hemorrhage
  90. Turbid CSF indicates increased __________ or _________.
    cellularity; protein conc
  91. What is the Pandy test?
    screening for Ig in CSF; + test is increased turbidity when mixed with carbolic acid
  92. Most CSF protein is from ____________.
    plasma albumin
  93. The major Ig in CSF is _________.
  94. What is the most frequent abnormality in CSF?
    increased protein
  95. 4 causes of increased protein conc in CSF.
    blood contamination, inflammation/space-occupying lesions disrupting BBB, inflammation causing increase intrathecal production of Ab, or both
  96. How are WBCs and RBCs counted in CSF?
    using a hemocytometer
  97. Causes of mild pleocytosis. (3)
    viral, trauma, vascular disease
  98. Causes of moderate pleocytosis. (2)
    fungal, protozoal
  99. Causes of severe pleocytosis. (2)
    bacterial, immune-mediated
  100. What cells are the major types in NORMAL CSF in dogs, cats, and horses? In cattle?
    • dogs, cats, horses: large mononuclear cells 
    • cattle: lymphocytes
  101. Neutrophilic pleocytosis is associated with _________, except __________.
    bacterial infections; Listeria
  102. Neurophilic pleocytosis indicates that ______ of the cells are neutrophils; it can be caused by... (5)
    >50%; bacterial infection, meningiomas, trauma/hemorrhage, vasculitis, meningitis
  103. Mononuclear pleocytosis indicates that _______ of the cells are large mononuclear cells; it can be caused by... (5)
    >75%; viral, fungal, rickettsial, granulomatous disease, subarachnoid hemorrhage
  104. Lymphocytic pleocytosis indicates that _______ of the cells are lymphocytes; it can be caused by... (7)
    >75%; viral, fungal, rickettsial, Listeria, granulomatous disease, subarachnoid hemorrhage, intracranial thrombosis, neoplasia
  105. Acute lead toxicity in calves and salt poisoning in pigs will cause _________ of the CSF.
    eosinophilic pleocytosis
  106. CNS ________ are the only neoplastic cells that can routinely be seen in CSF.
  107. __________ is more sensitive than visual inspection for etiologic agents in CSF.
  108. What is the most common fungal infection in the CSF?
    Cryptococcus neoformans