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Neuro Exam #1 > Intro to neuropath > Flashcards

Intro to neuropath Flashcards

1
Q

Discuss the significance the rough ER (aka Nissl substance)

A

…reflects high degree of active protein synthesis in neurons.

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2
Q

How does Nissl substance react to axotomy?

A

Central chromatolysis: 1) RER disaggregates 2) neuronal body balloons 3) cytoplasm becomes smooth 4) nucleus is displaced toward the periphery of the cell.

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3
Q

Discuss the use of silver stains in the histological study of the CNS

A

usually H&E stain (hematoxylin and eosin) is used for cellular details but it doesn’t stain neuronal processes so you need silver stains in which silver is deposited and then reduced to black metallic silver.

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4
Q

What is the significance of GFAP?

A

GFAP (glial fibrillary acidic protein) composes intermediate filaments in astrocytes. Antibodies against GFAP are commonly used to demonstrate reactive and neoplastic astrocytes.

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5
Q

How is myelin formed?

A

schwann cells and oligodendrocytes. composed of 70% lipids and 30% proteins.

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6
Q

Describe the role of microglia in CNS inflammation and repair

A

In response to damage they become activated, migrate to the site of the lesion, assume a different shape (inactivated have elongated nuclei and a small amount of cytoplasm with short processes. activated have large rod-shaped nuclei and ramified cytoplasm), undergo mitosis, and engulf foreign material. they express class 2 MHCs, function as APCs in inflammation, and play a role in regeneration of blood vessels after injury (by influencing migration of endothelial cells).

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7
Q

Describe the structure of the sarcolemma

A

sarcolemma is the cell membrane of a striated muscle fiber cell. Consists of a plasma membrane, which is a lipid bilayer, and an outer coat consisting of a thin layer of polysaccharide material (glycocalx) that contacts the basement membrane, which contains numerous thin collagen fibrils and specialized proteins such as laminin that provide a scaffold for the muscle fiber to adhere to.

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8
Q

Describe how key sarcolemma proteins are involved in the pathogenesis of muscular dystrophies

A

1) mutations of dystrophin = duchenne + becker 2) defects in sarcoglycan complex = limb girdle dystrophies 3) deficiency of merosin = congenital muscular dystrophies. 4) defects in b-dystroglycan-merson chain can cause muscular dystrophy.

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9
Q

Describe how type I and type II fibers are distributed in normal muscle

A

mixed like a checkerboard

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10
Q

Describe how type I and type II fibers are distributed in the denervation atrophy

A

in chronic denervation, type I and II equalize. So you get a clustered distribution rather than an intermixed distribution.

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11
Q

compare and contrast the differences between central and peripheral myelin

A

1) as far as composition they’re essentially identical. 2) however, peripheral myelin regenerates more efficiently (1 cell to 1 sheath) 3) also, there are significant differences in proteins between the two, which explains why PNS myelin does not cause central demyelination and vice versa.

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12
Q

describe the pathogenesis and pathological process of Wallerian degeneration, and where the most common site is clinically.

A

1) Axon is transected the portion distal to the transection degenerates. Both the axon and its surrounding myelin disintegrate because the nucleus-based source of energy metabolism is no longer available to the axon. corticospinal (pyramidal) tract. 2) Changes in the neuronal body = central chromatolysis 3) schwann cells distal to transection proliferate and make new myelin.

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13
Q

Is recovery faster in segmental or Wallerian degeneration?

A

…

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14
Q

what is neuropil?

A

fibrillary “matrix” of the cerebral gray matter. Formed by cellular processes of neurons and glial cells. These processes fit together tightly, leaving a minimal extracellular space. It is traversed by blood vessels.

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15
Q

What is the perivascular (Virchow-Robin) space?

A

As leptomeningeal vesels penetrate the brain, the subarachnoid space dips into CNS tissue around them, creating this space. This is accentuated in paraffin-embedded CNS tissue and appears as empty space. Extends down to the level of arterioles and venules.

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16
Q

what is the function of neuropeptides?

A

Involved in impulse transmission, regulation of neuronal cytoarchitecture, and as trophic factors. Include opioid peptides, substance P, hypothalamic releasing factors, gut hormones, pituitary peptides.

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17
Q

what is central chromatolysis?

A

reversible change that develops during repair of a neuron that has been disconnected from its target. Characteristics outlined in axonal transection question.

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18
Q

describe neurofilaments

A

longitudinally arranged 10 nm intermediate filaments in the neuronal cell body.

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19
Q

describe neurotubules

A

longitudinally arranged 20 to 26 nm tubules in the neuronal cell body. Consist of polymers of alpha and beta tubulin.

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20
Q

describe cross bridges

A

groups of tau protein and microtubule associated proteins (MAPs) that link neurotubules to one another and anchor them to cellular structures.

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21
Q

Describe the abnormal cytoskeleton of AD

A

abnormal filaments (paired helical filaments) appear in the cell body, forming neurofibrillary tangles (NFTs)

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22
Q

describe the ischemic or red cell neuron

A

This is the histological manifestation of irreparable cell necrosis. Takes up to 8-12 hrs to become recognizable. 1) neuron shrinks 2) becomes eosinophilic due to condensation of mitochondria 3) nuclei become pyknotic.

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23
Q

describe cytoplasmic lipofuscin

A

abnormal material that collects in neurons due to lysosomal enzyme deficiencies. Causes little or no functional damage.

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24
Q

Where do viral inclusions occur in HSV and CMV?

A

nucleus.

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25
Q

Where do inclusions occur in cytomegalic inclusion body disease and rabies?

A

cytoplasm.

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26
Q

describe classic neuritic plaques

A

This is the extracellular and distal manifestation of AD. Amyloid accumulates within brain and axonal or dendritic processes are found in a spherical arrangement around amyloid and represent a “disconnection of wires”

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27
Q

what is the most commonly used silver stain and what does it show?

A

bielschowsky stain, shows normal axons and dendrites. reveals lesions of AD.

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28
Q

what is synaptophysin?

A

synaptic vesicle protein that interacts with synaptobrevin

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29
Q

how do you demonstrate specific chemical components of nerve cells such as cytoskeletal proteins?

A

immunohistochemistry.

30
Q

what cell type are radial glia?

A

astrocytes

31
Q

What are rosenthal fibers? Where are they usually seen?

A

homogenous, eosinophilic, elongated, or globular inclusions in astrocytic processes. They have a filamentous and granular structure and contain GFAP. Seen old brain scars + low grade astrocytomas.

32
Q

What do mutations in GFAP cause? And how is this disease characterized?

A

Alexander disease, characterized by diffuse deposition of Rosenthal fibers, resuling in white matter degeneration and neurological dysfunction.

33
Q

describe some pathologies involving oligodendroglia

A

MS. can be infected by viruses in subacute sclerosing panencephalitis and PML. also demylinated in metachromatic leukodystrophy (lysosomal enzyme deficiency disorder).

34
Q

describe ependymal cells

A

relatively inert. have cilia. attached to a layer of dense material similar to basement lamina which merges with astrocytic glial processes under the ependyma. Form a loose barrier. in relevant pathologies (eg hydrocephalus) they’re disrupted and lost.

35
Q

neuronophagia

A

process in which degenerating neurons are encircled by microglial cells

36
Q

microglial nodules

A

when microglia form clusters around small foci of necrotic brain tissue.

37
Q

perimysium

A

this is the fibrocollagenous sheath that surrounds individual muscle fibers

38
Q

endomysium and its involvement in muscular dystrophy pathophys

A

this is the space between individual muscle fibers that carries capillaries. In muscular dystrophies, it increases and replaces lost muscle, causing muscles to stiffen.

39
Q

myofibril

A

this is the unit of contractile filaments in each myofiber. smallest unit.

40
Q

what is the importance of dystrophin and the dystrophin-associated complex (DAC)

A

These are the main components of the chain of proteins that attaches the contractile part of myofibers to the ECM.

41
Q

sarcolemma

A

cell membrane of muscle

42
Q

where does dystrophin lie and what is attached to?

A

under the sarcolemma, where its attached to cytoskeletal actin by its C-terminus and the N-terminus is bound to beta-dystroglycan.

43
Q

What are the transmembrane proteins composing the DAC?

A

dystroglycans and sarcoglycans

44
Q

what is beta-dystroglycan bound to?

A

merosin, the alpha 2-chain of the basement membrane protein laminin 2.

45
Q

Type 1 fibers

A

slow-red. rich in oxidative enzymes, mitochondria, myoglobin and lipid. capable of protracted slow action and clonic activity.

46
Q

Type 2 fibers

A

fast-white. rich in glycogen and glycolytic enzymes. capable of fast, powerful, tonic contraction..

47
Q

phosphocreatine

A

energy source for muscle. used to replenish ATP.

48
Q

creatine kinase (CK)

A

enzyme that moves phosphate from creatine phosphate to ADP, present in abundance in muscle. Biomarker for myonecrosis because it leaks out.

49
Q

motor unit

A

group of 100-200 myofibers all innervated by the same motor neuron. All fibers of a motor unit are of the same type (1 or 2)

50
Q

myopathy definition and how its characterized.

A

primary disease of muscle. characterized by proximal weakness, elevated CK, and characteristic EMG changes. muscular dystrophies and inflammatory myopathies. On path its characterized by myonecrosis and structural abnormalities.

51
Q

what does denervation atrophy cause?

A

distal weakness and atrophy and different EMG changes. CK is normal. On path, change in histochemical staining.

52
Q

describe myonecrosis/segmental response to muscle injury

A

segmental response to muscle injury. fibers necrose, are invaded by macrophages which remove debris. myonuclei from adjacent intact segments proliferate and initiate regeneration. Necrosis and regeneration go hand in hand but eventually one prevails. Lost muscle, such as in muscular dystrophies, is replaced by adipose tissue and collagen.

53
Q

what are the 2 basic types of reactions to muscle injury?

A

atrophy and myonecrosis/segmental response.

54
Q

what is endoneurium?

A

small amount of matrix present between individual axons

55
Q

what is perineurium?

A

sheath of special, fiber-like cells that ties axons of each fascicle together.

56
Q

what is epineurium?

A

connective tissue that surrounds the entire nerve trunk and gives off vascular connective tissue septa that traverse the nerve and separate fascicles from one another.

57
Q

size beyond which axons in the CNS and PNS are myelinated?

A

one micron

58
Q

describe structure of unmyelinated axons

A

covered by Schwann cell cytoplasm. no schwann cell membrane, of course.

59
Q

what are the 3 pathological patterns of neuropathy?

A

1) Wallerian degeneration 2) distal axonopahy 3) segmental demyelination

60
Q

what happens if PNS reconstruction following wallerian degeneration is not good?

A

traumatic neuroma. haphazard proliferation of collagen, Schwann cell processes, and axonal sprouts fill the gap.

61
Q

What causes Wallerian degeneration?

A

trauma, infarction of peripheral nerve (diabetic mononeuropathy, vasculitis), neoplastic infiltration.

62
Q

describe distal axonopathy

A

*disease begins in most distal part of nerves since the nerve is unable to keep up with metabolic demands. 1) axon and myelin degenerate first in most distal parts of axon 2) if abnormality persists, axon “dies back” 3) neurofilaments and organelles accumulate in the degenerating axon 4) axon becomes atrophic and breaks down

63
Q

what causes distal axonopathy?

A

drugs and industrial poisons damage some metabolic process.

64
Q

describe segmental myelination

A

1) breakdown and loss of myelin over a few segments 2) axon remains intact and there is no change in the neuronal body 3) this leads to decreased conduction velocity and conduction block 4) deficits are rapid but reversible because Schwann cells make new myelin. 5) HOWEVER, can lead to loss of axons and permanent deficits. 6) nerve shows thin-regenerating-myelin “onion bulbs”

65
Q

what neuropathies are characterized by segmental demyelination?

A

1) inflammatory demyelinative neuropathies 2) Charcot-Marie-Tooth disease

66
Q

what are “onion bulb” formations?

A

concentric layers of Schwann cell processes and collagen around an axon. This is caused by repetitive segmental demyelination and regeneration of myelin and can cause hypertrophic neuropathy

67
Q

hypertrophic neuropathy

A

gross thickening of peripheral nerves.

68
Q

sensory ataxia

A

Loss of coordination caused by loss of sensory input. It is caused by a lesion in the central axons of neurons in the gracile and cuneate tracts of the spinal cord.

69
Q

How do astrocytes react to injury?

A

astrocytes react to tissue injury by expansion of cytoplasmic volume and synthesis of intracytoplasmic intermediate glial filaments.

70
Q

How would you demonstrate synaptophysin?

A

immunohistochemistry

Neuro Exam #1 (23 decks)

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