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1

This pattern of neuronal cell injury leads to shrunken individual cell bodies and nuclei. They are prominently stained by eosin, leading to the term "red neurons."

Acute hypoxic/ischemic injury(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 860

2

These are round, faintly basophilic, PAS-positive, concentrically lamellated aggregates of polyglucosans that range between 5 and 50 micrometers, and are located wherever there are astrocytic end processes, especially in the subpial and perivascular zones, seen more frequently with advancing age.

Corpora amylacea (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 861

3

Cells which produce myelin in the CNS.

Oligodendrocytes (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 861

4

Cells which line the ventricles, and are located in the region of the obliterated central canal of the spinal cord.

Ependymal cells (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 861

5

These are responsible for the secretion of CSF. It has a specialized epithelial covering with a fibrovascular stroma that may contain meningothelial cells.

Choroid plexus (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 861

6

These are bone marrow-derived cells that function as the phagocytes of the CNS.

Microglia (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 861

7

It is the accumulation of excess fluid within the brain parenchyma. The brain is softer than normal and often appears to "overfill" the cranial vault. In generalized edema the gyri are flattened, the intervening sulci are narrowed, and the ventricular cavities are compressed.

Cerebral Edema (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 861

8

This occurs when the integrity of the normal blood-brain barrier is disrupted. With increased vascular permeability, fluid shifts from the vascular compartment into the intercellular spaces of the brain.

Vasogenic edema (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 861

9

This is due to an increase in intracellular fluid secondary to neuronal, glial, or endothelial cell membrane injury, as might be encountered in an individual with a generalized hypoxic/ischemic insult or with exposure to some toxins.

Cytotoxic edema(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 861

10

Refers to the accumulation of CSF leading to dilation of the ventricular system which resulted from an obstacle or disruption of flow seen most commonly at the foramen of Monroe or aqueduct of Sylvius.

Noncommunicating hydrocephalus (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 862

11

Refers to the accumulation of CSF leading to dilation of the ventricular system due to reduced resorption of CSF. All of the ventricular system is enlarged.

Communicating hydrocephalus (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 862

12

This refers to dilation of the ventricular system with a compensatory increase in CSF volume secondary to a loss of brain parenchyma, as may occur after infarcts or with a degenerative disease.

Hydrocephalus ex vacuo (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 862

13

This ccurs when unilateral or asymmetric expansion of a cerebral hemisphere displaces the cingulate gyrus under the edge of falx. This may be associated with compression of branches of the anterior cerebral artery.

Subfalcine (cingulate) herniation(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 862

14

This occurs when the medial aspect of the temporal lobe is compressed against the free margin of the tentorium. As the temporal lobe is displaced, the third cranial nerve is compromised, resulting in pupillary dilation and impairment of ocular movements on the side of the lesion ("blown pupil").

Transtentorial (uncinate) herniation (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 862

15

This refers to displacement of the cerebellar tonsils through the foramen magnum. This pattern of herniation is life-threatening, because it causes brain stem compression and compromises vital respiratory and cardiac centers in the medulla.

Tonsillar herniation (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 862

16

These linear or flame-shaped lesions usually occur in the midline and paramedian regions, which are hemorrhagic lesions that accompany transtentorial herniation. Presence of these lesion implies poor prognosis.

Duret hemorrhages(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 862

17

In the setting of this condition, the brain is swollen, with wide gyri and narrowed sulci. The cut surface shows poor demarcation between gray and white matter. Results from generalized reduction of cerebral perfusion, usually below systolic pressures of less than 50mmHg.

Global Cerebral Ischemia (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 863

18

These are wedge-shaped areas of infarction that occur in those regions of the brain and spinal cord that lie at the most distal fields of arterial perfusion. Usually seen after hypotensive episodes.

Border zone ("watershed") infarcts(TOPNOTCH)Robbins Basic Pathology, 9th ed., p. 1264

19

Pattern of necrosis seen in nonhemorrhagic infarcts of the brain.

Liquefaction necrosis(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 863

20

The most frequent cause of subarachnoid hemorrhage. It is a thin-walled outpouching of an artery. At the neck of the aneurysm, the muscular wall and intimal elastic lamina stop short and are absent from the aneurysm sac itself; the sac is made up of thickened hyalinized intima. The adventitia covering the sac is continuous with that of the parent artery

Saccular (berry) aneurysm(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 866

21

Patients with this type of intracranial hemorrhage complains of having "the worst headache I've ever had"/ thunderclap headache.

Subarachnoid Hemorrhage (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 866

22

Most common location for berry/saccular aneurysms.

Anterior communicating artery in the Circle of WIllis (40%)(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 867

23

This is a disease in which amyloidogenic peptides are deposit in the walls of medium- and small-caliber meningeal and cortical vessels, which results in the weakening of the vessel wall and increases the risk of hemorrhage.

Cerebral amyloid angiopathy (CAA) (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 863

24

Hemorrhages associated with cerebral amyloid angiopathy (CAA) due to involvement of the cerebral hemispheres?

Lobar hemorrhages(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 863

25

A type of vascular malformation which are characterized by of ectatic venous channels.

Venous angiomas (varices) (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 868

26

Most common location for berry aneurysms.

Anterior communicating artery in the Circle of WIllis (40%)(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 867

27

The involved vessels in this condition resemble a tangled network of wormlike vascular channels. Microscopically, they are enlarged blood vessels separated by gliotic tissue, often with evidence of prior hemorrhage.

Arteriovenous malformations (AVM)(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 868

28

A type of vascular malformation which are characterized by microscopic foci of dilated, thin-walled vascular channels separated by relatively normal brain parenchyma and occurring most frequently in the pons.

Capillary telangiectasias(TOPNOTCH)Robbins Basic Pathology, 8th ed., p 868

29

Minute aneurysms in vessels that are less than 300 micrometers in diameter, associated with chronic hypertension.

Charcot-Bouchard microaneurysms (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 868

30

This leads to accumulation of arterial blood between the dura and the skull. The expanding hematoma has a smooth inner contour that compresses the brain surface. Clinically, patients may experience a lucid interval between the moment of trauma and development of neurologic symptoms.

Epidural Hematoma (TOPNOTCH)Robbins Basic Pathology, 8th ed., p 870