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Sheet 1 Flashcards

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1
Q

Why are diseases that affect the brain always serious?

A

Because they may

leave permanent damage on the central nervous system.

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2
Q

The central nervous system is composed of two parts:

A

1) Central part
a) Brain
b) Spinal cord
2) Peripheral part: Related to the peripheral nerves

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3
Q

What is the functional unit of the CNS?

A

The neuron.

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4
Q

Neurons of different types and locations have distinct properties such as:

A

1) Functional roles
2) Distribution of their connections
3) Neurotransmitters used
4) Metabolic requirements
5) Levels of electrical
activity at a given moment.

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5
Q

What does the pattern of clinical signs and symptoms following injury depend on?

A

1) The pathologic process

2) The region of the brain involved

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6
Q

Why is the loss of neurons permanent?

A

Because mature neurons are incapable of cell division.

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7
Q

Which cells make up the glia?

A

1) Astrocytes

2) Oligodendrocytes

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8
Q

When do the features/changes of neuronal injury start to appear? When do they become obvious and clear?

A

12 hours after the injury; 24 hours after the injury.

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9
Q

Within 12 hours of an irreversible hypoxic-ischemic injury, insult, acute neuronal injury can be seen using which type of stain?

A

Hematoxylin and Eosin (H&E) staining.

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10
Q

What are the features of a neuronal injury?

A

1) Shrinkage of the cell body
2) Pyknosis of the nuclei
3) Nucleolus disappears
4) Loss of Nissl substance with intense eosinophilia of the cytoplam (“red neurons”)
5) Nuclei assumes the angulated shape of the shrunken cell body
6) Injured axons undergo swelling and show disruption of axonal transport
7) Spheroids (swellings) can be seen on H&E stains and can be highlighted by silver staining or immunohistochemistry
8) Central chromatolysis
9) Breakdown of BBB and variable degrees of cerebral edema (acute injury)
10) Intracellular inclusions
11) Intranuclear inclusions
12) Dystrophic neurities
13) Accumulation of complex lipids in cytoplasm and lysosomes.

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11
Q

What is Pyknosis?

A

(1) Clumping of nuclear material, (2) Dense in color, (3) Irregular in shape, (4) Smaller in size, and (5) Can be lost or fragmented

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12
Q

What is the Nissl substance?

A

Part of the rough endoplasmic reticulum (site of protein synthesis)

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13
Q

What is central chromatolysis?

A

1) Cell body enlargement and rounding
2) Peripheral displacement of the nucleus
3) Enlargement of the nucleolus,
4) Peripheral dispersion of Nissl substance

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14
Q

Destruction of the BBB is associated with:

A

Exposure of the tissue to more substances that may be injurious.

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15
Q

In which disease are Lewy bodies found?

A

Parkinson’s disease

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16
Q

In which disease are tangles found?

A

Alzheimer’s disease

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17
Q

Which virus causes intranuclear inclusions in all cells of the body (including neurons)?

A

CMV (Cytomegalovirus)

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18
Q

What are dystrophic neurities?

A

When neuronal processes become thickened and tortuous

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19
Q

If you see lipofuscin in neuronal cells, what does it indicate?

A

Previous exposure to an injurious agent.

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20
Q

What is the function of astrocytes?

A

Gliosis: Repair and scar formation in the brain

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21
Q

Astrocytes can undergo ___ and ___ in response to injury.

A

hypertrophy; hyperplasia

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22
Q

What are the features of a reactive astrocyte (Gemistocytic astrocyte)?

A

1) The nucleus enlarges and becomes vesicular
2) The nucleolus becomes prominent
3) The previously scant cytoplasm expands and takes on a bright pink hue
4) The cell extends multiple stout, ramifying processes.

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23
Q

Where can gemistocytic astrocytes be found?

A

1) Injured areas of the brain

2) Tumors (ex. Glioblastoma)

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24
Q

Fibroblasts participate in brain injury healing, except for:

A

Penetrating brain trauma or around abscesses.

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25
What are the features of fibrillary astrocytes?
1) The cytoplasm of reactive astrocytes shrink in size | 2) Cellular processes become more tightly interwoven.
26
When do reactive astrocytes become fibrillary astrocytes?
In longstanding gliosis
27
What are Rosenthal fibers?
Thick, elongated, and bright eosinophilic protein aggregates found in astrocytic processes in chronic gliosis and some low-grade gliomas
28
Fibrillary astrocytes and Rosenthal fibers can be seen in:
Injuries and tumors.
29
What is the function of oligodendrocytes?
Production of myelin.
30
What changes happen in oligodendrocytes in progressive multifocal leukoencephalopathy (PML)?
Viral inclusions with smudgy, homogenous appearing, and enlarged nuclei.
31
What are microglial cells?
Small, bone marrow derived, phagocytes of the CNS.
32
What is the function of microglial cells?
Activated microglial cells proliferate and become histologically prominent.
33
Microglial cells take on the appearance of activated macrophages in areas in the following conditions:
1) Demyelination 2) Organizing infarcts (leads to cell death/necrosis) 3) Hemorrhage 4) Rod cells (in infections)
34
Which disease do elongated nuclei (rod cells) develop in microglial cells?
Neurosyphilis or other infections.
35
What are microglial cells at sites of tissue injuries called?
Microglial nodules
36
What is the phagocytosing of neuronal cell injuries by microglial cells called?
Neuronophagia
37
What are ependymal cells?
They line the ventricular system and the central canal of the spinal cord.
38
Which pathogens can produce extensive ependymal injury and tumors?
CMV (Cytomegalovirus) and other viruses.
39
Because the ependymal cells line the ventricles, what is their abnormality manifested as?
Hydrocephalus
40
What is the choroid plexus?
It's a specialized epithelial covering that is continuous with the ependyma.
41
What is the ependyma?
The thin neuroepithelial lining of the ventricular system of the brain and the central canal of the spinal cord.
42
What is the function of the choroid plexus?
Secretion of the cerebrospinal fluid (CSF)
43
Disorders that may cause dangerous increases in brain volume within the fixed space of the skull include:
1) Generalized cerebral edema 2) Hydrocephalus 3) Mass lesions such as tumors.
44
What is cerebral edema?
The accumulation of excess fluid within the brain parenchyma.
45
What are the 2 types of edema?
1) Vasogenic edema | 2) Cytotoxic edema
46
What is vasogenic edema?
The integrity of the normal blood-brain barrier (BBB) is disrupted, allowing extravasation of vascular compartment proteins into the extracellular spaces of the brain.
47
What is cytotoxic edema?
An increase in intracellular fluid secondary to neuronal and glial cell membrane injury. (No obvious underlying cause).
48
Depending on the underlying cause, vasogenic edema can be:
1) Localized | 2) Generalized
49
What is an example of localized vasogenic edema?
Increased vascular permeability due to inflammation or tumors
50
Which neuronal and glial cell membrane injuries can lead to cytotoxic edema?
1) Generalized hypoxic-ischemic | 2) exposure to some toxins.
51
What are the characteristics of an edematous brain?
1) It is softer than normal | 2) Appears to overfill the cranial vault
52
What are the characteristics of a generalized edematous brain?
1) Flattening of the gyri 2) Narrowing of intervening sulci 3) Compression of ventricular cavities
53
What absorbs the CSF?
Arachnoid granulations
54
What regulates CSF volume?
The balance between rates of generation and resorption
55
What is hydrocephalus?
The accumulation of excess CSF within the ventricular system
56
What causes hydrocephalus?
1) Impaired flow or resorption | 2) Overproduction of CSF (choroid plexus tumors, rare)
57
What are the 3 types of hydrocephalus?
1) Noncommunicating hydrocephalus 2) Communicating hydrocephalus 3) Hydrocephalus ex vacuo
58
What is noncommunicating hydrocephalus?
A localized obstacle to CSF flow within the ventricular system = A portion of the ventricles enlarges while the remainder does not.
59
What is the most common cause of noncommunicating hydrocephalus?
Masses (tumors) obstructing the foramen of Monro or compressing the cerebral aqueduct
60
What is communicating hydrocephalus?
The entire ventricular system is enlarged
61
What is the most common cause of communicating hydrocephalus?
Reduced CSF resorption
62
What is hydrocephalus ex vacuo?
A compensatory increase in CSF volume following the | loss of brain parenchyma
63
What can cause hydrocephalus ex vacuo?
1) Infarcts | 2) Degenerative diseases
64
What happens if hydrocephalus develops in infancy BEFORE the cranial sutures close?
The head enlarges
65
What happens if hydrocephalus develops AFTER the cranial sutures close?
1) Ventricular expansion | 2) Increased intracranial pressure
66
True or false: | The head circumference changes increases in hydrocephalus after closing of the cranial sutures.
False
67
When does herniation occur?
When the volume of tissue and fluid inside the skull increases beyond the limit permitted by compression of veins and displacement of CSF resulting in increased intracranial pressure
68
What subdivides the cranial vault?
Rigid dural folds (falx and tentorium).
69
What does herniation lead to?
Pinching and vascular compromise of the compressed tissue = infarction = more swelling = more herniation.
70
The herniated part is swollen because:
The vessels are compressed
71
What is compromised in herniations?
Absorption of fluid
72
What are the 3 types of herniations?
1) Subfalcine (cingulate) herniation 2) Transtentorial (uncinate) herniation 3) Tonsillar herniation
73
What is the most serious type of herniation?
Tonsillar herniation
74
What is a subfalcine (cingulate) herniation?
It occurs when unilateral or asymmetric expansion of a cerebral hemisphere displaces the cingulate gyrus under the edge of falx.(falx is part of the brain membrane).
75
What is a subfalcine (cingulate) herniation associated with?
Compression of the anterior cerebral artery so any area supplied by the vessel can be affected.
76
What is a transtentorial (uncinate) herniation?
It occurs when the medial aspect of the lobe is compressed against the free margin of the tentorium.
77
Which lobe is displaced by a transtentorial (uncinate) herniation?
Temporal lobe
78
Which nerve is compromised by a transtentorial (uncinate) herniation?
Third cranial nerve
79
What are the consequences of a transtentorial (uncinate) herniation (nerve-wise)?
``` Loss of vision due to: a) Pupillary dilation b) Impaired ocular movements on the side of the lesion. ```
80
Which artery is compressed by a transtentorial (uncinate) herniation?
Posterior cerebral artery
81
What are the consequences of a transtentorial (uncinate) herniation (artery-wise)?
Ischemic injury to tissue supplied by that vessel, including the primary visual cortex.
82
If the amount of displaced temporal lobe is large enough, the pressure on the midbrain can compress the ____ against the tentorium, resulting in ___ ipsilateral to the side ___(opposite/of) the herniation, so-called false localizing sign.
contralateral cerebral peduncle; hemiparesis; of.
83
The compression of the contralateral cerebral peduncle creates a deformation known as:
Kernohan’s notch
84
Progression of transtentorial herniation is often accompanied by:
Duret hemorrhages: linear or flame-shaped hemorrhages in the midbrain and pons
85
What causes Duret hemorrhages?
Involvement of the small veins and arteries supplying the upper brain stem that can be torn during the herniation
86
Where do Duret hemorrhages usually occur?
In the midline and paramedian regions
87
What is tonsillar herniation?
Displacement of the cerebellar tonsils through the foramen magnum (narrow = compression)
88
Why are tonsillar herniations life threatening?
1) Causes brain stem compression | 2) Compromises vital respiratory and cardiac centers in the medulla.

CNS Patho (8 decks)

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