Week 0: PATHOLOGY [part 1] Flashcards

1
Q

occurs when the medial aspect of the temporal lobe is compressed against the free margin of the tentorium.

A

Transtentorial (uncinate, mesial temporal) Herniation

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2
Q

When the extent of herniation is large
enough the contralateral cerebral peduncle may be compressed,
resulting in hemiparesis ipsilateral to the side
of the herniation; the compression in the peduncle in
this setting is known as the

A

Kernohan Notch

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3
Q

Progression
of transtentorial herniation is often accompanied by secondary
hemorrhagic lesions in the midbrain and pons,
termed

A

Duret Hemorrhages

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4
Q

accumulation of excess fluid within

the brain parenchyma.

A

Cerebral edema

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5
Q

is an increase in

CSF volume within all or part of the ventricular system

A

Hydrocephalus

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6
Q

severe malformation
with a flattened, disorganized segment of
spinal cord, associated with an overlying meningeal
outpouching.

A

Spinal dysraphism or spina bifida

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7
Q

spinal dysraphism that is asymptomatic bony defect

A

spina bifida occulta

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8
Q

extension
of CNS tissue through a defect in the vertebral
column

A

myelomeningocele

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9
Q

applies when there is only

a meningeal extrusion

A

meningocele

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10
Q

refers to a diverticulum of malformed

brain tissue extending through a defect in the cranium.

A

encephalocele

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11
Q

overall recurrence rate for a neural tube defect

in subsequent pregnancies has been estimated at

A

4 to 5 percent

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12
Q

malformation of the anterior end of the

neural tube, with absence of most of the brain and calvarium.

A

anencephaly

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13
Q

flattened remnant of disorganized
brain tissue with admixed ependyma, choroid
plexus, and meningothelial cells

A

area cerebrovasculosa

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14
Q

The absence of cortical gyri defines this abnormality,

A

lissencephaly

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15
Q

characterized by small, unusually

numerous, irregularly formed cerebral convolutions.

A

polymicrogyria

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16
Q

a spectrum of malformations characterized
by incomplete separation of the cerebral hemispheres
across the midline.

A

holoprosencephaly

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17
Q

Holoprosencephaly is

associated with ____________ as well as other genetic syndromes.

A

trisomy 13

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18
Q

absence of the white matter
bundles that carry cortical projections from one hemisphere
to the other

A

agenesis of the corpus callosum

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19
Q

bat wing deformity on radiologic imaging

A

misshapen lateral ventricles d/t agenesis of the corpus callosum

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20
Q

consists of a small posterior fossa, a misshapen midline
cerebellum with downward extension of vermis through
the foramen magnum (Fig. 28-7), and, almost invariably,
hydrocephalus and a lumbar myelomeningocele

A

Arnold-Chiari malformation (Chiari type II malformation)

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21
Q

less severe disorder in
which low-lying cerebellar tonsils extend down into the
vertebral canal

A

Chiari type I malformation

22
Q

characterized by an enlarged
posterior fossa. The cerebellar vermis is absent or present
only in rudimentary form in its anterior portion

A

Dandy Walker Malformation

23
Q

hypoplasia
of the cerebellar vermis with apparent elongation
of the superior cerebellar peduncles and an altered
shape of the brainstem;

A

Joubert’s Syndrome

24
Q

Molar Tooth sign on imaging

A

Joubert’s syndrome

25
Q

characterized by expansion of the

ependyma-lined central canal of the cord

A

Hydromyelia

26
Q

formation of a fluid-filled cleft-like cavity in the

inner portion of the cord

A

Syringomyelia

27
Q

formation of a fluid-filled cleft-like cavity in the

inner portion of the cord that extends to the brainstem

A

Syringobulbia

28
Q

histologic appearance is destruction of the adjacent gray and white matter,
surrounded by a dense feltwork of reactive gliosis

A

neurologic malformations in general

29
Q

Infarcts may occur in the supratentorial periventricular

white matter

A

perventricular leukomalacia

30
Q

The principal functional unit of the central nervous system

CNS

A

Neuron

31
Q

Neurons requires a continuous supply of ___ and _____ for its metabolic needs

A

glucose and oxygen

32
Q

spectrum
of changes that accompany acute CNS hypoxia/ischemia or
other acute insults and reflect the earliest morphologic markers
of neuronal cell death (

A

acute neuronal injury/ red neurons

33
Q

morphologic patterns of red neurons

A

enlargement of the cell body, pyknosis of the nucleus, disappearance of the
nucleolus, and loss of Nissl substance, with intense eosinophilia
of the cytoplasm.

34
Q

axonal reaction to injury is manifested by

A

enlargement and
rounding up of the cell body, peripheral displacement of the
nucleus, enlargement of the nucleolus, and dispersion of Nissl
substance from the center to the periphery of the cell (central
chromatolysis).

35
Q

may occur as a manifestation of

aging, when there are intracytoplasmic accumulations complex lipids (lipofuscin), proteins, or carbs

A

neuronal inclusions

36
Q

Abnormal intranuclear inclusion seen in herpetic infection

A

Cowdry body

37
Q

Abnormal intranuclear inclusion seen in rabies infection

A

Negri body

38
Q

most important histopathologic indicator of

CNS injury, regardless of etiology

A

Gliosis

39
Q

These cells have multipolar, branching cytoplasmic pro
cesses
that emanate from the cell body and contain glial
fibrillary acidic protein (GFAP),

A

Astrocytes

40
Q

they contribute to barrier functions controlling the flow of macro
molecules
between the blood, the cerebrospinal fluid (CSF) and the brain

A

Astrocytes

41
Q

are thick, elongated,
brightly eosinophilic, irregular structures that occur
within astrocytic processes, and contain two heat-shock
proteins (αB-crystallin and hsp27) as well as ubiquitin

A

Rosenthal fibers

42
Q

are mesoderm-derived phagocytic cells that

serve as the resident macrophages of the CNS.

A

Microglia

43
Q

the ciliated columnar epithelial cells

lining the ventricles

A

ependymal cells

44
Q

an increase in intracellular fluid secondary
to neuronal, glial, or endothelial cell membrane
injury, as might be encountered in someone with a generalized
hypoxic/ischemic insult or with a metabolic
derangement that prevents maintenance of the normal
membrane ionic gradient

A

Cytotoxic edema

45
Q

occurs especially
around the lateral ventricles when an increase in intravascular
pressure causes an abnormal flow of fluid from the
intraventricular CSF across the ependymal lining to the
periventricular white matter.

A

Interstitial Edema (hydrocephalic edema)

46
Q

if the ventricular system is obstructed and does not
communicate with the subarachnoid space, as may occur
because of a mass in the third ventricle, it is called

A

non communicating or obstructive hydrocephalus

47
Q

ventricular system is in communication
with the subarachnoid space, and there is enlargement of
the entire ventricular system.

A

Communicating Hydrocephalus

48
Q

compensatory increase in ventricular

volume secondary to a loss of brain parenchyma.

A

Hydrocephalus ex vacuo

49
Q

Displacement of brain tissue past rigid dural folds (the falx and tentorium) or through openings
in the skull because of increased intracranial pressure

A

Herniation

50
Q

occurs when unilateral or assymetric expansion of a cerebral hemisphere displaces the cingulate gyrus under the falx

A

Subfalcine (cingulate) herniation