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SBM Neuro > 10-17 Intro to NeuroPATH > Flashcards

10-17 Intro to NeuroPATH Flashcards

1
Q

Nissl stain stains for?

A

RER

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2
Q

Cajal silver stain?

A

neurons and axons

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3
Q

Stain for astrocytes?

A

IHC (immunohistochemistry) for GFAP (glial fibrillary acidic protein)

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4
Q
  1. Changes in Neuronal Cell Body (Perikaryon): histo appearance of ischemic ∆s/stroke?
A

Contracted neuron with hypereosinophilia b/c of anoxic lactic acidemia of cytoplasm (“red – dead neuron”) and pyknosis of nuclei. Severely damaged neurons will eventually disappear.

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5
Q
  1. Changes in Neuronal Cell Body (Perikaryon): histo appearance of Neuronal atrophy
A

gradual shrinkage of cell body and withering of its dendritic tree (e.g. neurodegenerative diseases, disuse atrophy, transsynaptic atrophy).

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6
Q
  1. Changes in Neuronal Cell Body (Perikaryon): histo appearance of Neuronal loss
A

Can only be appreciated microscopically when there is approximately 30% cell loss; to determine fewer losses, computerized counting machines are now being used.

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7
Q
  1. Changes in Neuronal Cell Body (Perikaryon): histo appearance of chromatolysis
A

In Nissl preparations, Nissl granules disappear; sign of retrograde degeneration following injury or transection of axons. It can also be seen in some toxic-metabolic disorders without axonal damage, as in pellagra for instance.

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8
Q
  1. Changes in Neuronal Cell Body (Perikaryon): histo appearance of Ferrugination
A

mineralization, incrustations): Mineral (Ca and Fe) deposits in damaged neurons

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9
Q
  1. Changes in Neuronal Cell Body (Perikaryon): histo appearance of neuronophagia
A

Phagocytosis of a degenerated neuron by macrophages.

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10
Q
  1. Changes in Neuronal Cell Body (Perikaryon): s/sx and cause of pellagra
A

**niacin (vitamin B3) deficiency (less commonly tryptophan)

“the four Ds”: diarrhea, dermatitis, dementia and death

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11
Q
  1. Changes in Neuronal Cell Body (Perikaryon): lipofuscin
A

—‘wear-and-tear’ pigment insoluble mixture of lipids and proteins that accumulate during the course of aging.
—Some cells such as in the inferior olivary nuclei will exhibit Lipofuscin earlier than in Purkinje cells, which are relatively resistant to such an accumulation.
—If a lipofuscin-like material (ceroid) is seen in neurons in early life, it indicates a form of storage disease, “ceroid-lipofuscinosis.”

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12
Q
  1. Changes in Neuronal Cell Body (Perikaryon): histo appearance of lipid storage material
A

according to the site of catabolic enzymatic block, various sphingolipids or gangliosides accumulate in perikaryon causing the cells to distend, enlarge, and assume a globular shape.

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13
Q
  1. Changes in Neuronal Cell Body (Perikaryon): neurofibrillary tangles
A

are bundles of abnormal filaments seen in such disorders as in Alzheimer’s disease (flame-shaped one = AD)

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14
Q
  1. Changes in Neuronal Cell Body (Perikaryon): inclusions
A 
may be nuclear and/or cytoplasmic
—‘Lewy bodies’ in Parkinson's
—Bunina bodies in ALS
—‘Cowdry type A’ inclusions in herpes encephalitis
—several bright red in Rabies
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15
Q
  1. Changes in Neuronal Processes: Wallerian degeneration
A

degeneration of an axon distal to INJURY. If the axon is myelinated, the myelin sheath will fragment as a secondary effect.

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16
Q
  1. Changes in Neuronal Processes: “Dying Back:
A

degeneration of the most distal segments of an axon due to inability of the cell body to maintain adequate axoplasmic flow or produce needed NUTRIENTS seen in some toxic neuropathies and certain neurodegenerative diseases (system degeneration).

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17
Q
  1. Changes in Neuronal Processes: axonal spheroids
A

focal bulbous swellings of axons, usually the result of sublethal injury.

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18
Q
  1. Changes in Neuronal Processes: demyelination
A

a) primary insult to myelin sheath or myelin forming cell (oligodendroglia in
CNS and Schwann cell in PNS) or (b) secondary to degeneration of axons as in Wallerian or
dying-back.

19
Q
  1. Changes in Neuronal Processes: dendritic abnormalities
A

—causing decr I/O signals in neuron
—abnormal spine configuration or loss.
—Loss of dendritic branches is often seen in
developmental disorders, both congenital and acquired.
—dendritic pruning seen in HIV dementia, ant horn cells in ALS

20
Q

astrocytes

A

respond to almost any stimulus, first by enlarging (reactive astrocytes) and then retracting fibrous astrocytes) when the injurious process subsides.

21
Q

glosis and brain scarring

A

The cell processes of fibrous astrocytes form a network (glial scar or gliosis) that mends an injured area. Most scars in the CNS are glial; fibrous scars formed of fibroblasts only occur in abscess walls or are post traumatic when meninges (mesodermal tissue) are driven into brain tissue

22
Q

Alzheimer’s Type II glia

A

—NOT seen in A.D.
—glia that proliferate and undergo a alteration in conditions where the blood and CSF ammonia levels are elevated, such as in hepatic encephalopathy, and when serum electrolytes are out of balance.
—nuclei are large w/ clear karyoplasm and chromatin distributed under nuclear membrane.
—Sometimes line up = “kissing glial”.

23
Q

oligodendrocytes

A

form and maintain CNS myelin; their destruction will lead to demyelination as in progressive multifocal leukoencephalopathy (PML), a viral (JC virus) condition that selectively ‘colonizes’ oligodendrocytes.
—1 cell—> myelinates many neurons

24
Q

ependymal and chroid plexus cells

A

glial derivation arising from the neuroectoderm. Ependymal cells line ventricles and maintain equilibrium between cerebrospinal and interstitial fluids of the brain. They are tall columnar ciliated cells but show regional variations in cell configuration reflecting modified function, e.g., over the choroid plexuses they acquire a more cuboidal appearance, have prominent microvilli and develop the ability to SECRETE CSF.
—irrelevant in almost all neuropathological conditions
—Their response to most insults is to die.
—little or no regenerative capacity

25
Q

microglia

A

NOT GLIAL AT ALL: specialized monocyte/macrophage which arises in the bone marrow and populates the CNS before birth.
—assist in the remodeling of the fetal CNS by phag’ing cells that apoptose.
—post natal: small, dense, elongated nuclei without identifiable cytoplasm.
—Special cytosol stains show it to be arranged as thin branches radiating from the nuclear zone.
—establish individual, non- overlapping territories. —comprise 8-10% of all CNS cells, and are inconspicuous until reaction is req’d in the neural parenchyma.
—respond to myriad: neuronal death, trauma, inflammation/infection, tumor infiltration, and infarction.

26
Q

reactive possibilities of microglia

A 
become macrophages (so called "gitter" cells) when there is necrotic material to engulf.
—present antigen and secreting cytokines in inflamma or infx.
—assume a highly elongated "rodcell"morphology in some chronic conditions like CNS syphilis.
—proliferate and assume cell surface molecular phenotype of reactive MOs when there is neuronal death of tumor infiltration in the vicinity.
27
Q

Schwann Cells

A

—similar functions to astrocytes, oligodendrocytes, and microglia in the PNS.
—myelinate motor and sensory axons
—important components of the synapse at the NMJ
—ingest tissue debris and promote regeneration after injury.
—can proliferate as neoplasms (Schwannomas) or after injury in a hyperplastic fashion (traumatic neuroma).

28
Q

areas most susceptible to anoxia

A

—pyramidal neurons of a) hippocampus (esp CA1 region) & b) third lamina in the cortex
—Purkinje cells of the cerebellum show ischemic changes much earlier and more severe than any other region of the brain
—

29
Q

theories for hippocampus being so susceptible to anoxia

A
  1. Regional vascular compromise such as kinking, stretching of feeding vessels secondary to brain swelling - a frequent complication of anoxia
  2. Differences in regional energy requirements
  3. Glutamate toxicity
30
Q

pathophys of glutamate toxicity

A
  • lots of Glut. in presynaptic terminals is released during anoxia/ischemia while reuptake particularly by astrocytes is decrease, incr interstitial
    —[Glut] causes neurotoxicity by binding to NMDA receptors —> opens Na+ and Ca++ channels —> osmotic swelling mediated by entry of Na+ into neurons and delayed neuronal death by the entry of Ca++.
    —Pyramidal neurons in CA1 may possess more NMDA receptors which may explain their vulnerability in anoxia.
31
Q

Vitamin b1

A

thiamine

32
Q

Vitamin B1 deficiency

A

Thiamine (B1) def. causes Wernicke’s encephalopathy, results in acute destructive changes in the mammillary bodies, wall of the third ventricle and the floor of the fourth ventricle

33
Q

Vitamine B12

A

cyanocobalamin

34
Q

Vitamine B12 deficiency

A

cause destruction of the white matter in the dorsal and lateral columns of the spinal cord.

35
Q

Wilson’s disease

A

cavitations resulting from necrosis are particularly prominent in the striatum where copper (Cu) levels are increased

36
Q

Monro-Kellie doctrine

A

v.intracranial (constant) = v.brain + v.CSF + v.blood + v.mass lesion

37
Q

vasogenic vs. cytotoxic edema

A
  1. vasogenic: (BBB) is compromised, (some neoplasms or infections): excess fluid —> intercellular spaces
  2. cytotoxic: damage to cell: glia or neurons enlarge due to ∆s in cell membranes and ion/H20 flux. seen w/ hypoxia/ischemia or some chemical intoxications.
    —Usually both types contribute to overall brain swelling
38
Q

raised ICP (in mmH2O)?

A

> 200mmH2O w/ pt recumbent

39
Q

herniations

A
  1. tonsillar herniation: cerebellar tonsils -> foramen magnem -> compress brainstem -> cardiopulm arrest
  2. subfalcine herniation: cingulate gyrus herniates under falx -> compress Ant. cerebral a. -> ischemia
  3. uncal: uncus into area between cerebellum and brain stem -> compress a) CN III (down and out eyes w/ dilated pupils b) PCA (infarcted occipital lobe) c) pull on paramedian artery along brain stem -> direct hemorrhages on brain stem
40
Q

hydrocephalus

A

the excess accumulation of CSF in the ventricular system. Most cases of hydrocephalus are due to impaired flow through the ventricular system or impaired resorption of CSF. Increased production of CSF can occur, though, in rare choroid plexus tumors.

41
Q

non-communicating hydrocephalus

A

refers to enlargement of focal area of the ventricular system due to blockage.

42
Q

communicating hydrocephalus

A

generalized enlargement of the entire ventricular system.

43
Q

hydrocephalus ex vacuo

A

dilated ventricular system secondary to loss of brain parenchyma.

SBM Neuro (29 decks)

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