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Neuro unit 1 > neuropathology > Flashcards

neuropathology Flashcards

1
Q

neuropil

A

The fibrillary “matrix” of the cerebral gray matter, formed by the cellular extensions (processes) of the neurons and glial cells.

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2
Q

perivascular (Virchow-Robin) space

A

where subarachnoid space dips into CNS tissue

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3
Q

The large rounded vesicular nucleus and often
prominent nucleolus in neurons reflect what?The large rounded vesicular nucleus and often
prominent nucleolus in neurons reflect what?The large rounded vesicular nucleus and often
prominent nucleolus in neurons reflect what?

A

the high metabolic activity and protein synthetic demands of the neuron.

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4
Q

Most metabolically active cell in entire body

A

neurons

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5
Q

relate the size of soma and length of axon

A

They parallel each other: larger soma=longer axon

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6
Q
  1. Understand the significance of the rough endoplasmic reticulum (RER aka Nissl substance) and how it reacts to axotomy.
A

Reflects active protein synthesis. Axotomy (severing the axon) causes the RER to disaggregate and the neuronal body balloons. The cytoplasm becomes smooth and the nucleus is displaced toward the periphery of the cell. This appearance, which is called central chromatolysis, is a reversible change that develops during repair of a neuron that has been disconnected from its target

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7
Q

What do hematoxylin, eosin, silver and luxol fast blue stain. What is immunohistochemistry used for?

A

hematoxylin: DNA/RNA. Eosin: protein. Luxol: myelin. Silver: axons/dendrites (Bielschowsky stain, shows normal axons anddendrites and reveals also the lesions of Alzheimer’s disease). Immunohistochemistry: cytoskeletal proteins and synaptophysin

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8
Q

Neuron response to injury

A
  1. total necrosis (ischemic neuron). 2. chromatolysis (injury to neuron usually at level of the axon, with subsequent death of neuron or regrowth of axon). 3. Acquisition of viral particles within nucleus or cytoplasm (viral infections). 4. Acquisition of abnormal material within cytoplasm (neurodegenerative processes, storage disorders)
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9
Q

What do ischemic neurons look like

A

“red dead” - lloss of basophilic nissl substance results in eosinophilia. Shrunken nucleus. Some cells are more vulnerable (purkinje cells)

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10
Q

What does chromatolysis look like

A

A swollen cell body as the neuron attempts to regrow/repair a damaged axon

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11
Q

What do you see in idiopathic parkinsons disease in neurons?

A

Lewy bodies in neurons of the substantia nigra compacta

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12
Q

What do you see in Alzheimers disease in neurons

A

neurofibrillary tangles (seen with silver histochemical stain

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13
Q

Transection of axon causes what?

A

Results in necrosis of axon distal to the transection. This is known as Wallerian degeneration. Swollen axonal processes at site of injury. Also, axon may disconnect from their synapse and aggregate around beta amyloid material in brain parenchyma (plays role in alzheimers)
Results in necrosis of axon distal to the transection. This is known as Wallerian degeneration. Swollen axonal processes at site of injury. Also, axon may disconnect from their synapse and aggregate around beta amyloid material in brain parenchyma (plays role in alzheimers)
Results in necrosis of axon distal to the transection. This is known as Wallerian degeneration. Swollen axonal processes at site of injury. Also, axon may disconnect from their synapse and aggregate around beta amyloid material in brain parenchyma (plays role in alzheimers)

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14
Q

most common site of wallerian degeneration

A

corticospinal (pyramidal) trac

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15
Q
  1. Know the basic components of the neuronal cytoskeleton and how alterations of some of these components are associated with neurodegenerative diseases.
A

10nm neurofilaments and 20nm neurotubules (alpha and beta tubulin). Neurotubules are linked together by tau protein and microtubule associated proteins (MAPs). Neurotubules and neurofilaments form the cytoskeleton. Phosphorylation of neurofilaments influencs structural stability and speed of axoplasmic flow. In Alzheimer’s disease, abnormal filaments (paired helical filaments) appear in the perikaryon, forming neurofibrillary tangles (NFTs).

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16
Q

Materials that neurons accumulate with time and disease

A

Cytoplasmic lipofuscin cause little or no functional damage. Lipid storage materials, viral particles, and abnormal cytoskeleton alteration damage neuronal function.

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17
Q

What are neuritic plaques

A

extracellular and distal manifestation of Alzheimer’s disease. Amyloid accumulates within brain, then axonal and dendritic processes with abnormal cytoskeleton arranges spherically around the amyloid.

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18
Q

Role of astrocytes

A

Have receptors for neurotransmitters, astrocyte procsses surround synapses where they may play role in metabolism/inactivation of neurotransmitters, structural support, radial glia (development), form scars (brain parenchyma lacks fibroblasts), monitor ionic environment (redistributes K), induction of blood brain barrier, ammonia metabolism, possibly antigen presenting cells,

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19
Q
  1. key protein of astrocytes.
A

GFAP is a protein that makes up the intermediate filaments. Rosenthal fibers (homogeneous, eosinophilic, elongated, or globular inclusions in astrocytic processes) also contain GFAP and are seen in old brain scars.

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20
Q

Alexander disease

A

mutations of GFAP. Causes diffuse deposition of Rosenthal fibers, resulting in white matter degeneration and neurological dysfunction

21
Q

How do astrocytes responst to tissue injury

A

By expansion of cytoplasmic volume and synthesis of intracytoplasmic intermediate glial filaments (GFAP)

22
Q

Can astrocytes fill in large holes of tissue damage

A

No, they do not produce extracelular collagen like fibroblasts but rather undergo cytoplasmic expansion and cell process extension

23
Q

Regenerative capacity of oligodendroglia

A

limited

24
Q
  1. Understand how myelin is formed and what cells make myelin in the CNS and PNS.
A

oligodendroglia serve as source of myelin. Sensitive to irradiation

25
Q

Ependymal cells structure and function

A

ciliated cells that line ventricular spaces, with little evidence of proliferation or regeneration under pathological condition. May play role in local CSF movement. Btw cells are junctions, but this does not prevent passage of certain particles (thus is not the only barrier to CSF-extracellular fluid communications)

26
Q
  1. Understand the role of microglia in CNS
A

intrinsic, “first line” phagocytic system within the brain. Following CNS injury, resting microglial cells become activated, migrate to the site of the lesion, assume different shapes, undergo mitosis, and engulf foreign material. Monocyts from blood can also enter CNS and become phagocytes, and the two types of phagocytes cant be differentiated morphologically. microglia/monocytes are target for AIDS, express class II MHC, are antigen presenting cells, play role in regeneration of blood vessels.

27
Q

neuronophagia

A

microglia encircling degenerating neurons

28
Q

microglial nodules

A

microglia form clusters around small foci of necrotic brain tissue

29
Q

List steps in CNS tissue response to traumatic injury

A
  1. hemostasis: platelet adhesion, fibrin deposition, leukocytes release signaling molecules. 2. inflammation: BBB reestablished, reduced inflammatory cell recruitment, debridement by macrophages, microglia and astrocytes, axonal breakdown. 3. repair: gliosis. Astrocytes encircle lesion, no ECM depostion, limited angiogenesis, astrocytes prevent axonal regeneration. 4. remodelling: dense gliosis, no lesion filling, neurons protected by gliosis
30
Q
  1. Describe the structure of the sarcolemma and key intracellular, transmembrane, and extracellular proteins associated with it
A

Fasciculus is made of muscle fibers made of myofibrils (actin and myosin). Myofibrils are bound to ECM by dystrophin and dystrophin-associated complex (made of dystroglycans and sarcoglycans). Dystrophin lies under sarcolemma (cell membrane of muscle) and is bound to B-dystroglycan which is bound to merosin (part of the basement membrane protein laminin 2)

31
Q

Muscular dystrophies

A

Defects in the dystrophin-dystroglycan-merosin chain cause progressive muscle damage. Mutations of
dystrophin are the basis of Duchenne and Becker muscular dystrophies. Defects of the sarcoglycan complex cause some of the limb girdle dystrophies. Deficiency of merosin is found in some congenital muscular dystrophies.Defects in the dystrophin-dystroglycan-merosin chain cause progressive muscle damage. Mutations of
dystrophin are the basis of Duchenne and Becker muscular dystrophies. Defects of the sarcoglycan complex cause some of the limb girdle dystrophies. Deficiency of merosin is found in some congenital muscular dystrophies.

32
Q
  1. Describe how type I and type II fibers are distributed in normal muscle and in the denervation atrophy.
A

type 1 (slow-red): rich in oxidative enzymes, mitochondria, myoglobin and lipid. Slow action and clinic activity. type 2 (fast-white): rich in glycogn and glycolytic enzymes, capable of fast, powerful, tonic contractions, but more fatiguable. Both types are present in all muscles. In acute denervation atrophy, type II fibers are targeted (b/c they are more fatiguable and die earlier). in Chronic denervation atrophy, type I and II proportion equalize.

33
Q

energy usage/reserves for muscle

A

ATP hydrolysis is immediate source of energy. Phsophocreatine is used indirectly by creatine kinase which moves phosphate from phosphocreatine to ADP. CK leaks out into serum during muscle damage

34
Q

motor unit

A

100-200 myofibers, all innervated by the same
motor neuron. All fibers of a motor unit
are of the same histochemical type, i.e. either type 1 or type 2.

35
Q

Categories of muscle disease

A

Myopathy (primary disease of muscle), is characterized by proximal weakness, elevated CK, and characteristic EMG changes. This broad group includes the muscular dystrophies and inflammatory
myopathies. Denervation atrophy most often causes distal weakness and atrophy, and different
EMG changes. CK is normal.

36
Q

Muscle’s reaction to injury

A

Atrophy and myonecrosis. During necrosis, adjacent myonuclei proliferate and regenerate fibers, but in disease either necrosis or regeneration will predominate. Lost muscle (if not replaced by muscle) is replaced by adipose and collagen. Denervation causes atrophy.

37
Q

Endo-peri-and epineurium

A

Endoneurium is between individual axons. The perineurium is a sheath of special, fiber-like cells that ties the axons of each fascicle together. Epineurium is the 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.

38
Q
  1. What are the differences between central and peripheral myelin?
A

In the CNS, myelin is produced by oligodendroglial cells and in the PNS by Schwann cells. Each oligodendrocyte makes multiple segments of myelin that wrap around many axons. Each Schwann cell makes one segment of myelin. Peripheral myelin regenerates more efficiently. unmyelinated axons in periphery are covered by schwann cell cytoplasm but not myelin. 70% lipids, 30% protein in both CNS and peripheral myelin, but the proteins are different btw the two

39
Q

Patterns of peripheral neuropathy

A

Wallerian degeneration, distal axonopathy, and segmental demyelination.

40
Q

Describe wallerian degeneration

A

When an axon is transected, its distal part, including the myelin sheath, undergoes a series of changes leading to its complete structural disintegration and chemical degradation. The RER disaggregates, neuronal body balloons, cytoplasm becoms smooth, nucleus is displaced towards periphery. This is called central chromatolysis (activation of protein synthesis to regenerate axon). Then, the proximal stump elongates and new myelin is made. and degree of regeneration depends on how well the cut ends are put together

41
Q

clinical signs of nerve regeneration

A
  1. autonomic (sweating). 2. sensation. 3. motor
42
Q

Traumatic neuroma

A

If reconstruction during wallerian degeneration is not good, a haphazard proliferation of collagen, Schwann cell processes, and axonal sprouts fill the gap

43
Q

Which types of neuropathies exhiit wallerian degeneration

A

those that are caused by trauma, infarction of peripheral nerve (diabetic mononeuropathy, vasculitis) and neoplastic infiltration

44
Q

distal axonopathy

A

degeneration of axon and myelin develops first in the most distal parts of the axon and, if the abnormality persists, the axon “dies back”. Causes distal sensory loss and weakness. Drugs, pesticides, organic phosphates and solvents cause this. It results from an inability to keep up with metabolic demands of axon

45
Q

Segmental demyelination

A

breakdown and loss of myelin over a few segments. The axon remains intact and there is no change in the neuronal body. Decreased conduction velocity and conduction block. Deficits are reversible (schwann cells make new myelin), but demyelination can cause loss of axons and permanent deficits.

46
Q

Neuropathies characterized by segmental demyelination

A

acute and chronic inflammatory demyelinative neuropathies and Charcot-Marie-Tooth disease

47
Q

Onion bulb formation

A

Concentric layers of Schwann cell processes and
collagen around an axon caused by repetitive segmental demyelination and regeneration of myelin and can cause gross thickening of peripheral nerves (hypertrophic neuropathy). Hallmark of Charcot-marie-tooth disease

48
Q

How to distinguish btw axonal vs demyelinating processes

A

nerve conduction studies: demyelinative neuropathy show slowing of conduction velocities while axonal neuropathy show low action potential amplitudes

Neuro unit 1 (17 decks)

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