Np 1: Cellular Neuropathology

Front 1

Cell Body Alterations:
Acute ischemic or hypoxic damage leads to what histologic changes? What is the likely outcome?

Back 1

Eosinophilia and pyknotic nuclei. These changes are thought to be irreversible and lethal.

Front 2

Cell Body Alterations:
Atrophy:
1) What histological changes are seen?
2) In what diseases is this seen?

Back 2

1) Non eosinophilia shrinkage
2) Neurodegenerative diseases, Alzhiemer's, Parkinson's, Huntington's

Front 3

Cell Body Alterations:
Chromatolysis:
1) What is it?
2) What are the histologic characteristics?
2) What can happen after chromatolysis and where is this seen?

Back 3

1) Damage to axon results in loss of Nissl substance ie. rough ER
2) Loss of Nissl substance and hypertrophy of cell body.
3) There can be axonal regrowth from site of damage typically in the peripheral nervous system

Front 4

Cell Body Alterations:
Storage disease:
1) What is seen?

Back 4

1) Abnormal accumulation of lipids, proteins, carbs, etc, leading to enlarged distorted geometry

Front 5

Cell Body Alterations:
Inclusions
1) What is seen? Examples?

Back 5

1) Abnormal nuclear or cytoplasmic structures: such as metabolites, viral porteins, lewy bodies, neurofbrillary tangles?

Front 6

Cell Body Alterations:
Lifpfuscin:
1) What is it?
2) What causes it?

Back 6

1) Insoluble accumulation of a mix of proteins, lipids and minerals in neurons and astrocytes
2) In normal aging

Front 7

Cell Body Alterations:
Neuronphagia:
1) What is it?
2) When is it seen?

Back 7

1) Phagocytosis of neurons
2) After damage, hypoxic or ischemic, or from viral infection

Front 8

Axon:
1) Wallerian Degeneration:
2) Dying back degeneration: Seen when?
3) Spheroid? When is it seen? What is included in spheroid?

Back 8

1) Dying of axon distal to insult site
2) Degeneration of distal axon followed by more proximal damage seen in toxic peripheral neuropathies
3) Focal enlargement of an axon due to any type of damage. They contain mixtures of lysosomes, mitochondria, neruofliaments and other cytoplasmic stuff. Usually due to slowing of axoplasmic transport.

Front 9

Dendrite
1) Hypoplasia? Ex: of diseases?
2) Atrophy? Seen in what diseases?

Back 9

1) Inadequate development of dendrite branching seen in MR (Ex: congenital hypothyroidism)
2) Reduction in volume and surface of dendritic branches, seen in neurodegenerative diseases

Front 10

Neuropil: What is it?
Nueritic plaques: Consist of what? Seen where?
Status spongiosis?

Back 10

-Unmyelinated nueronal processes.
-Dying axons, dendrities, beta amyloid plaques, microglia and astocytes EC
-Vacuoles in neuropil due to swollen neuronal and astrocytic processes.

Front 11

Astrocytes:
1) Hypertrophy and hyperplasia is a response to what?
2) What histological changes are seen? and when?

Back 11

1) Damage, trauma, ichemic
2) Pink cytoplasm either form
a) imbibing plasma proteins and fluid in short term when BBB is down or
b) filling up with intermediate filaments in the long term

Front 12

Alzheimer Type II Astrocytes:
1) Histologic appearance?
2) Seen in what diseases?

Back 12

1) Swollen, lucent nucleus and swollen cytoplasm in gray matter
2) In patients with chronic or acute liver disease

Front 13

Astrocyte Inclusions: The following contain what and occur in which diseases?
1) Rosenthal fibers
2) Corpora amlacea
3) Viral Inlusions

Back 13

1) Eosinophilic, with intermediate filaments and small heat shock proteins found in low grad pilocytic type astrocytomas
2) spherical accumulations of polyglucosan which increase with age in subentricular and subpial locations and in glial scars
3) CMV

Front 14

After damage to the CNS what other roles due astrocytes take on?

Back 14

They become phagocytic

Front 15

Ependymal cells: Basic characteristics?
1) What is cell loss due to and what are the consequences?
2) Neoplasias possible

Back 15

Single cell layer, cuboidal, ciliated epithelium that line ventricles
1) Many noxious stimula and leads to loss of ependymal lining of ventricle and proliferation of subependymal astrocytes (granular ependymitis)

Front 16

Microglia:
1) From where are they derived?
2) Functions?

Back 16

1) Bone marrow and enter CNS during development
2) Unclear, but following damage they turn into macrophages plus with lesions of BBB macrophages from monocytes elsewhere in circulation enter CNS. Microglia are also the APCs of the CNS.

Front 17

Endothelial Cells of CNS:
1) Response to ischemia?
2) What other pathologic changes can occer to the endothelial cells?

Back 17

1) Hypertrophy and hyperplasia also seen in vicinity of primary and metastatic neoplasms.
2) Cell loss, and fibrotic and hyalin thickening of vessel wall.

Front 18

Choroid plexus:
1) Function
2) 2 histologic features?

Back 18

1) make CSF via untra filtrate of blood
2) a) epithelium surrounds blood vessel stock and is derived from ectoderm
b) stalk is made of mesenchymal tissue and leak capillaries go through mesenchymal tissue to be filtured by choroid epithelium.