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NS2 Test 2 > Chapter 28 Part 1 > Flashcards

Chapter 28 Part 1 Flashcards

1
Q

Acute neuronal injury

A
  • accompanies acute CNS hypoxia/ischemia insult
  • red neurons-12-24 hours after insult–shrinkage of cell body, pyknosis of nucleus, disappearance of nucleolus, loss of Nissl substance (chromatolysis), intense eosinophilia of cytoplasm
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2
Q

Chronic Neuronal injury

A
  • Characteristic feature-cell loss (selectively involving functionally related groups of neuron
  • reactive glial changes-best indicator at early stages
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3
Q

Axonal reaction

A
  • Change in cell body during regeneration of the axon-best seen in anterior horn cells
  • increased protein synthesis associated with axonal sprouting
  • enlargement of cell body, peripheral displacement of nucleus, dispersion of nissl substance from center to periphery of cell
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4
Q

Neuronal inclusions

A
  • Manifestation of aging
  • genetic disorders of metabolism
  • viral infection
  • degnerative diseases
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5
Q

Viral infections–neuronal inclusions

A
  • Herpes-Cowdry bodies
  • Rabies-Negri bodies
  • CMV-in nucleus and cytoplasm
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6
Q

most important histopathologic indicator of CNS injury

A

gliosis

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7
Q

Gliosis

A
  • hypertrophy and hyperplasia of astrocytes
  • nuclei of astrocytes enlarge, become vesicular, develop prominent nucleoli
  • gemistocytic astrocytes-eccentric nucleus, swollen cytoplasm
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8
Q

Alzheimer type II astrocyte

A
  • in longstanding hyperammonemia–chronic liver disease, wilson disease, metabolic disorders of urea cycle
  • large nucleus, intranuclear glycogen, chromatin
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9
Q

Rosenthal fibers

A
  • thick, elongated, brightly eosinophiic, irregular structures that occur within astrocytic processes
  • in regions of long-standing gliosis
  • characteristic of pilocytic astrocytoma
  • Alexander disease (leukodystrophy)
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10
Q

Corpora Amylacea

A
  • polyglucosan bodies
  • round, faintly basophilic, PAS-positive
  • located where there are astroctyic end processes
  • occur in old age
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11
Q

Lafora bodies

A

-in cytoplasm of neurons in myoclonic epilepsy

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12
Q

What are microglia?

A

-resident macrophages of CNS

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13
Q

Microglia respond to injury by doing what 4 things?

A
  • proliferating
  • developing elongate nuclei (rod cells)
  • forming aggregates around small foci of tissue necrosis (microglial nodules)
  • congregating around cell bodies of dying neurons (neuronophagia)
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14
Q

Glial cytoplasmic inclusions

A
  • primarily alpha-synuclein

- found in multiple system atrophy

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15
Q

What are ependymal cells?

A

-ciliated columnar epithelial cells lining the ventricles

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16
Q

Ependymal granulations

A
  • small irregularities on ventricular surfaces due to disruption of ependymal lining and proliferation of subependymal astrocytes
  • due to infiltration or dilation of ventricular system
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17
Q

Pressure within cranial cavity rises in 3 clinincal settings:

A
  • generalized brain edema
  • increased CSF volume (hydrocephalus)
  • focally expanding mass lesion
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18
Q

2 main pathways of edema formation in brain

A
  • vasogenic edema (increased vascular permeability)

- cytotoxic edema (increase in intracellular fluid secondary to neuronal, glial or endothelial cell membrane injury

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19
Q

Gneralized edema-brain structure

A

-gyri flattened, sucli narrowed, ventricular cavities compressed

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20
Q

Interstitial edema (hydrocephalic edema)

A

-increase in intravascular pressure causes an abnormal flow of fluid from the intraventricular CSF across the ependymal lining to the periventricular white matter

21
Q

Non-communicating/obstructive hydrocephalus

A

-if ventricular system is obstructed and doesn’t communicate with subarachnoid space

22
Q

Communicating hydrocephalus

A
  • ventricular system is in communication with subarachnoid space
  • enlargement of the entire ventricular system
23
Q

Hydrocephalus ex vacuo

A

compensatory increase in ventricular volume secondary to brain atrophy

24
Q

What is a subfalcine (cingulate) herniation? what does it compress?

A
  • cingulate gyrus under falx

- anterior cerebral a

25
Q

What is a transtentorial herniation? What does it compress?

A
  • medial aspect of temporal lobe is compressed against tentorium
  • CN3
  • PCA
26
Q

Kernohan notch

A
  • when the herniation is large enough, the contralateral cerebral peduncle may be pressed
  • results in hemiparesis ipsilateral to side of herniation (in trantentorial herniation)
27
Q

duret hemorrhage

A

secondary hemorrhagic lesions in midbrain and pons that accompany progression of transtentorial herniation

28
Q

Tonsillar herniation

A
  • cerebellar tonsils through foramen magnum

- brain stem compression–life threatening

29
Q

Spina bifida (spinal dysraphism)

A
  • asymptomatic–spina bifida oculta

- neural tube does not close all the way

30
Q

myelomeningocele

A
  • extension of CNS tissue through defect in vertebral column
  • usually lumbosacral region
  • motor and sensory deficits in lower extremity
  • superimposed infection that extends into the cord
31
Q

meningocele

A

-only meningeal extrusion through defect in vertebral column

32
Q

encephalocele–what is it? Risk factor?

A
  • malformed brain tissue extending through a defect in the cranium
  • most common in posterior fossa
  • risk factor- folate deficiency during 1st week of gestation
  • neural tube closure–complete by day 28
33
Q

Anencephaly

A
  • malformation of anterior end of neural tube
  • absense of brain and calvarium
  • disrupted at 28 days
34
Q

area cerebrovasculosa

A

remains in forebrain place (in anencephaly)

-flattened remnant of disorganized brain tissue

35
Q

neurons from germinal matrix zone to cerebral cortex–2 paths

A
  • radial migration (become excitatory neurons)

- tangential migration (become inhibitory neurons)

36
Q

lissencephaly

A

reduction in number of gyri

37
Q

agyri

A

no gyrial pattern-extreme case

38
Q

lissencephaly- 2 general patterns

A
  • type 1: smooth surfaced form-mutations that disrupt the signaling for migration and cytoskeletal motor proteins that drive migration of neuroblasts
  • type 2-rough/cobblestoned surfaced from–disrupt the stop signal for migration–mutations in enzymes that place sugars onto proteins
39
Q

polymicrogyria

A
  • small, numerous, irregularly formed cerebral convolutions
  • gray matter with 4 layers with entrapment of meningeal tissue at point of fuse that would otherwise be by the cortical surface
40
Q

neuronal heterotopias

A
  • group of migrational disorders that are associated with epilepsy
  • presence of collections in neurons in inappropriate locations along the pathway of migration
41
Q

periventricular heterotopias–mutation?

A
  • gene encoding filamin A–actin binding protein–responsible for assembly of complex meshwork of filaments
  • DCX (dbl cortin)- on X chromosome-results in lissencephaly in males and subcortical band heterotopias in females
42
Q

Holoprosencephaly-severe and less severe cases? associated with?

A
  • incomplete separation of cerebral hemispheres across midline
  • severe- midline facial abnormalities
  • less severe- arhinencephaly- absence of olfactory CNs
  • associated with trisomy 21
  • mutations in SHH signaling pathway
43
Q

Agenesis of corpus callosum

A
  • absense of white matter bundles that carry cortical projections from 1 hemisphere to the other
  • Bat wing deformity- misshapen lateral ventricles
44
Q

Arnold-Chiari malformation (type II)

A
  • misshapen midline cerebellum with downward extension of vermis through foramen magnum
  • hydrocephalus, lumbar myelomeningocele
45
Q

Chiari-type 1 malformation

A
  • less severe
  • low-lying cerebellar tonsils extend down into vertebral canal
  • can be symptomatic because of impaired CSF flow and medullary compression
46
Q

Dandy- walker malformation

A
  • enlarged posterior fossa
  • cerebellar vermis absent or present in rudimentary form
  • large midline cyst in its place
  • expanded, roofless 4th ventricle
47
Q

Joubert syndrome

A
  • hypoplasia of cerebellar vermis with elongation of superior cerebellar peduncles and altered shape of brainstem
  • “molar tooth sign” on imaging
48
Q

hydromyelia

A

-expansion of ependyma- lined central canal of cord

49
Q

syringomyelia–what is it and when does it manifest?

A
  • fluid filled cavity in inner portion of cord
  • may extend into brainstem–syringobulbia
  • can be associated with chiari malformations, intraspinal tumors, traumatic injury
  • destruction of adjacent gray and white matter; gliosis
  • manifests in 2-3 decade of life–loss of pain and temp in UE

NS2 Test 2 (16 decks)

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