Basic neuropathology

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  1. Tissue stains
    • 1) H&E = pink w/ blue dots
    • 2) Cresyl violet- nissl substance
    • - Luxol fast blue - glia
    • 3) Bielschowkys silver- fiber neurons
    • 4) GFAP- immunohistochemistry (glia tumors)
  2. Chromatolysis
    • Neuronal reaction
    • acute axon injury -> perikaryon -> swelling & peripheral displacement of nucleus & nissl substance
    • Regeneration of the axon

    Caused by: acute infection, toxic, vascular, or metabolic changes
  3. Red neuron
    Neuronal reaction after acute injury that leads to necrosis or apoptosis.

    • shrinkage, pyknosis of nucleus(dense chromatin), triangular, cytotoxic edema, eosinophilia, loss of nissl bodies
    • H & E stain 12 -24 hours after irreversible hypoxic insult.
    • WHERE: hippocampus, neocortex, purkinje cells
  4. Chronic ischemia
    • Neuronal reaction
    • cork screw axons with microglia infiltration
  5. Nonperfused brain
    • acidophilic neurons, vascular proliferation
    • neurophagy via scavenger cells -> microglia scar & iron deposition
  6. neuronal atrophy
    • Neuronal reaction
    • end stage
    • accumulation of lipfuscin, distortion, dead neuron
    • If seen histologically = prolonged death
  7. numeric atrophy
    >30% depopulation in a given section
  8. Trans-synaptic degeneration
    • neuronal reaction (neuronal atrophy)
    • dendrite degeneration -> loss of afferent connection
    • WHERE: lat geniculate bodies (optic nerve damage)
    • - mammillary bodies (degen of fornix)
    • - neurons of gracile & cuneate (degen of post spinal cord)

    • Microscopically: binuclear nueron
    • - fenestrated neuron
  9. Neuronal hypertrophy
    • Neuronal reaction (trans-synaptic finding)
    • binuclear
    • neurofibrillary degeneration
    • fenestrated neuron
  10. Ferrugination
    • Iron deposit
    • SEEN IN:
    • Chronic trauma(boxers)
    • Old infarcts
    • Stage III syphilis
  11. Viral inclusions
    • CMV inclusion
    • Herpes cowdry bodies
    • oligodendrocytes with viral intranuclear inclusions
    • intracytoplasmic negri (rabies)
  12. Alzheimers
    Pakinsons
    Creutzfeldt-Jakob disease
    • Intracyoplasmc inclusions and highly resistant to degradation.
    • Alzheimers- neurofibrillary tangles
    • Parkinsons - Lewy bodies
    • Creutzfeldt-Jakob disease- vacuolization of perikaryon & neuronal cell processes in the neuropil
  13. Tay sachs diease
    • Neurolipid accumulation
    • Ganglioside
  14. Niemann Pick
    • Neurolipid accumulation
    • sphingomyelin
  15. Gaucher
    • Neurolipid accumulation
    • Glucocerbroside
  16. Gliosis
    local proliferation of astrocytes which leads to hypertrophy and hyperplasia
  17. Protoplasmic astrocytes vs fibrous astrocytes
    • Protoplasmic = intial repair
    • fibrous = later repair
  18. Anisomorphic vs Isomorphic
    • Anisomorphic = cortical scars
    • Isomorphic = white matter
  19. Reactive gliosis vs astrocytic gliosis
    • Reactive gliosis:
    • Hypertrophy of cytoplasmic processes
    • inc production of GFAP

    • Astrocytic gliosis:
    • hypertrophy and hyperplasia of astrocytes
  20. Gemistocytic gliosis
    Bright pink, somewhat irregular swath around an eccentric nucleus, from which emerge numerous stout, ramifying processes.

    • Found near tumors or areas of necrosis
    • or in tissue destruction & repair
  21. Copoar amylacea
    • Glucose polymers inclusion of astrocytes
    • Located in subpial, subependymal, and perivascular, and olfactory tracts.
  22. rosenthal fibers
    • Astrocytes cytoplasmic inclusion bodies.
    • densely compacted glial intermediate filaments with entrapped cytosolic proteins and form in long standing astrogliosis.
  23. Oligodendrocytes reaction to injury
    • Viral inclusion in progressive multifocal leukoencephalopathy.
    • Multiple system atrophy- glial cytoplasmic inclusions composed of a-synulein.
  24. Ependymal cells to injury
    • Lines ventricles.
    • Disruption leads to prolferation of subependymal astrocytes --> irregularities of ventricular surface.
    • CMV is a cause
  25. 3 types of alzheimers glia
    Type I (astrocytes) - multinucleated, eosinophilic, giant cells. WHERE: white matter

    Type II (liver glia)- nuclei > 20Mm & liver disease related(chronic liver disease, Wilsons disease, or hereditary metabolic disorder of urea cycle. Lobular nucleus & thick membrane

    Type III glia - devoid of cytoplasm. naked nuclei glia.
  26. How do microglia turn into foamy cells
    • activated into rod cells - lipid accumulation -> foamy cells
    • Also form microglial nodules (aggreagates around tissue necrosis)
    • neuronophagia (congregation around cell bodies of dying neurons)
  27. Types of brain edema
    • Vasogenic
    • cytotoxic
    • interstitial
  28. Brain edema
    What causes it
    What does it cause
    • BY: no lymphatic drainage & damage to BBB
    • CAUSES: ischemia & herniation
  29. Focal cerebral edema
    Unilateral
  30. Brain swelling after global edema
    Widened gyri, engorged veins, compressed sulci.
  31. TBI
    • Traumatic brain injury
    • disruption of brain functions with 1 or more:
    • LOC
    • loss of memory
    • AMS
    • Focal neurological changes
  32. 2 main complications of blunt trauma
    • Primary: trauma is the main cause
    • results in Diffuse axonal injury
    • Secondary: Blunt trauma leads to something else that causes brain problems
    • - Intracranial hematoma, edema, herniation, infection, infarction
  33. Penetrating Trauma
    • Functional impairments related to site of injury
    • Spinal cord transection or crush injury
  34. DAI definition
    • Small hemorrhagic lesions & diffuse damage to axons
    • No fracture involved
    • Microscopically: axon is swollen & looks like neuron (retraction ball) Present 12-24 hours later
  35. DAI grading
    • Grade I = DAI
    • Grade II = DAI & hemorrhage in corpus callosum
    • Grade III = DAI, hemorrhage in corpus callosum & lesions to DLR brainstem
  36. Concussion definition
    • altered consciousness after blunt head trauma
    • Presents with:
    • Transient LOC
    • Paralysis
    • Siezures
    • Recovery can take hours to days
  37. Contusion defintion
    • Blunt trauma with microhemorrhage without cavity formation
    • No hematoma present and continuity is preserved
    • Clincal:
    • LOC
    • transient --> permanent focal neurological defect
    • INC ICP
    • Coup vs countercoup
  38. Contusion timeline
    • DAI- 24 hours
    • Cerebral edema - 3 days
    • Delayed subdural hematoma ischemic injury- years
  39. Brain commotion
    • Pathology of concussion
    • Involves: Dysfx of reflexes
    • altered consciousness
    • widespread depolarization
    • no morphological findings
  40. Extrdural hemorrhage
    • Epidural hematoma caused by middle meningeal artery ->inc ICP -> mass effect
    • Course: drowsy-> coma-> death
  41. Subdural hemorrhage
    • small trauma -> veins damaged -> fibroblastic organization or cyst formation -> attracts water -> edema -> Inc ICP -> herniation or cerebral ischemia
    • Clinical: Biphasic LOC
  42. Post concussion symptoms
    • headache
    • irritability
    • dizziness
    • dec concentration
    • memory problems
    • fatigue
    • visual disturbance
    • Noise sensitivity
    • judgement problems
    • anxiety & depression
  43. Caput Hemorrhage
    • Birth Injury
    • Between skin & epicranial aponeurosis
    • Crosses midline
    • asymptomatic
    • gradually resolves
  44. cephalhematoma
    • Birth injury
    • collection of blood between Periosteum and skull
    • Common over parietal or occipital bones
    • limted by skull sutures -> does not cross midline
    • may lead to anemia or jaundice
    • gradually resolves
  45. Subgaleal hemorrhage
    • Birth injury
    • Collection of blood between epicranial aponeurosis & periosteum of skull
  46. Intracranial hemorrhage
    • Intracerebral bleeding from dural sinuses or brain substances
    • devastating
  47. Periventricular leukomalacia
    • Holes in white matter surrounding the ventricle.
    • Caused by change in blood flow or infection.
  48. Multicystic encephalopathy
    Formation of large multicoular cavities throughout the cerebral hemispheres

Card Set Information

Author:
lazzsant
ID:
126942
Filename:
Basic neuropathology
Updated:
2012-01-12 23:31:03
Tags:
Martinez
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Description:
Neuropathology
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