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NS2 Exam 2 > Robbins Ch. 28 > Flashcards

Robbins Ch. 28 Flashcards

1
Q

Acute Neuronal Injury: -what causes this? -earliest marker of what process? -timing?

A

-caused by depletion of glucose, O2, or trauma -earliest morphological marker of neuronal cell death - Red neurons evident by 12-24 hours after insult

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2
Q

Morphology of red neurons

A

-shrinkage of the cell body -pyknosis of nucleus -disappearance of nucleus -loss of nissl substance -INTENSE EOSINOPHILIA

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3
Q

What would you see in a chronic neuronal injury?

A

-accumulation of abnormal protein aggregates

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4
Q

what is seen when neurons are cut?

A

axonal reaction: enlargement and rounding up of the cell body, increased protein syn, enlargement of the nuc, dispersion of Nissl substance from the center to the periphery (central chromatolysis)

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5
Q

Astrocytes: -what do they do? -contain what filament?

A
  • they act as metabolic buffers and detoxify the brain; also contribute to the bbb -contain GFAP
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6
Q

Gliosis: -most important indicator of what? -characterized by what? -what changes are seen in astroyctes? -what is a name for these astrocytes

A

-most important indicator of CNS damage -characterized by hypertrophy and hyperplasia of astrocytes -astrocyte nucleus enlarges, becomes vesicular, and develops prominent nuclei -cytoplasm expands to a bright pink forming swaths around the eccentric nucleus that form numerous stout ramifying processes “gemistocytic astrocytes:

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7
Q

Rosenthal fibers: -characteristics -commonly seen w/ what tumors -contain which HSPs

A

-thick, elongated, brightly eosinophilic, irregular structures that occur within astrocytic processes -commonly seen w/ slow growing benign tumors -found in regions of long standing gliosis and characteristic of PILOCYTIC ASTROCYTOMA -contain ab-cystallin, HSP27 -also contain ubiquitin

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8
Q

Alexander dz -mutations in GFAP cause? -where do rosenthal fibers aggregate?

A

-leukodystrophy due to mutations in GFAP -contain lots of RFs in periventricular, perivascular, and subpial locations

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9
Q

Capora amylacea:

  • also called ____ bodies
  • shape/characteristics/staining?
  • what causes them?
A
  • AKA polyglucosan bodies
  • round faintly basophilic, periodic acid schiff positive, concentrically lamellated
  • increase w/ age and thought to be from ND dzs
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10
Q
  • oligodendrocyte response to injury
  • microglia response to injury
A
  • oligodendrocytes–> injury or apoptosis of oligos is a feature of acquired demyelinating disorders and leukodystrophies
  • Microglia–> respond by 1. proliferating 2. developing elongated nuclei 3. forming aggregates around small foci of tisssue necrosis (microglial nodules) 4. congregfating around cell bodies of dying neurons (neuronophagia)
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11
Q
  • oligodendrocytes harbor viral inclusions in which dz?
  • oligos have inclusions of a-synuclein in what dz?
A
  • viral inclusions in PML
  • a-synuclein inclusion in MSA
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12
Q

Cerebral edema:

-characteristics of gyri, ventricular cavities

A

gyri narrowed, ventricular cavities are compressed

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13
Q
  • where are microglia derived from
  • surface markers
A

mesoderm derived

CR3 CD68

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14
Q
  • vasogenic edema:
  • what fluid?
  • whats happening to the bbb?
  • brain lymphaticw
  • often follows what type of insult
A

increased ECF in the brain from BBB disruption and increased vascular permeability

  • problem is made worse by paucity of lymphatics in the brain
  • vasogenic edema often follows an ischemic injury
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15
Q

cytotoxic edema:

  • which fluid?
  • injury from what
A
  • increase in intracellular fluid secondary to neuronal, glial, or endothelial cell membrane injury
  • might be encountered in someone w/ a generalized hypoxic/ischemic insult, or with a metabolic derangement that prevents maintenance of the normal membrane gradient
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16
Q

interstitial edema

  • occurs where?
  • when does this occur?
A

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

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17
Q

Hydrocephalus

communicating vs non communicating

A

-communicating: the ventricular system is in communication w/ the subarachnodi space and t_here is enlargement of the entire ventricular system_

- non communicating: ventricular system is obstructed and does not communicate w/ the subarachnoid space–> may occur because of a mass in the third ventricle

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18
Q

Hydrocepalus ex vacuo:

-refers to a compensatory increase in ____

A

compensatory increase in ventricular volume seconeary to a loss of brain parenchyma

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19
Q

Herniation:

  • subfalcine
  • leads to compression of which a.
A
  • asymmetric expansion of the cerbral hemisphere displaces the cingulate gyrus under the falx
  • compression of the ACA
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20
Q

transtentorial (uncinate) herniation:

  • which lobe is compressed against the tentorium?
  • CN at risk?
  • a. at risk?
  • what is kernohan notch, and how does it happen?
  • duret hemorrhages
A
  • medial aspect of the temporal lobe is compressed against the tentorium
  • cn III can become compromised–> pupillary dilation impairment of Ex Occ movement
  • PCA–> ischemia of visual cortex
  • contralateral cerebral peduncle can also become compressed resulting in hemiparesis ipsilateral to the side of herniation
  • duret hemorrhages–> bleeds of midbrain/ pons
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21
Q

Tonsillar herniation:

  • what is displaced
  • why life threatening?
A

-cerebellar tonsils through the foramen magnum, life threatening because it compresses the brainstem and vital respiratory/cardiac centers

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22
Q

Encephalocele:

  • occurs most often where?
  • but can also occur throug cribriform plate, what is this known as?
  • risk factors
A
  • diverticulum that extends out of a defect in the cranium, most often occurs in the posterior fossa, but can occur through the cribriform plate–> known as nasal glioma (misnomer; not a tumor)
  • risk factors: previous pregnancy that was affected and folate deficiency during the first few weeks of gestation
23
Q

Forebrain anomalies:

  • Radial migration: which neurons? mediated by which protein?
  • transgential migration: which neurons?
A

forebrain anomalies are caused by asymmetric migration of neurons while they are proliferating

  • radial migration is for excitatory neurons and is due to the reelin protein
  • transgential migration for inhibitory neurons
24
Q

Microcephaly

-risk factors

A

-FAS, HIV-1 acquired in utero

25
Q

Lissencephaly

-type 1 vs type 2

A

reduction or no gyri

  • type 1 is smooth surfaced and is associated w/ disrupted signaling of the motor proteins that drive migration of neuroblasts
  • type 2 is rough surfaced and is commonly associated with genetic alterations that disrupt the stop signal for migration
26
Q

polymicrogyria:

  • what is it?
  • induced by?
A

small numerous irregularly formed cerebral convolutions with entrapment of the meningeal tissue at points of fusion that would have been the cortical surface

-induced by localized tissue injury toward the end of neural migration

27
Q

Neural heterotopias:

  • associated with what disorder
  • what happens to neurons during migration
  • mutations in which genes
A
  • associated w/ epilepsy
  • collections of neurons in the wrong locations along the pathway of migration
  • mutations in filamin A, DCX
28
Q

Holoprosencephaly:

  • incomplete separation of?
  • facial abnormalities?
  • associated w/ which trisomy?
  • defects in which pathway
A

incomplete separation of the 2 hemi. across the midline

severe forms can cause facial abnormalities including cyclopia or arrhinencephaly

  • associated with trisomy 13 (patau)
  • defects in sonic hedgehog
29
Q

agenesis of corpus collusum

  • what does it look like?
  • missing which gyrus
  • associated w/
A

-has a bat wing deformity where the lateral ventricles are misshapen, commonly associated with retardation

30
Q

Arnold-chiari malformation type II

-characteristics/abnormalities

A
  • small posterior fossa, misshapen midline cerebellum w/ downard extension of vermis through the foramen magnum, hydrocephalus, and a lumbar myelomeningocele
  • less commonly can include caudal displacement of the medulla, malformation of the tectum, aqueductal stenosis, and hydromelia
31
Q

Chiari type 1 malformation:

  • severity
  • abnormalities present
  • symptoms caused by
A
  • less severe than an arnold chiari type II
  • cerebellar tonsils extend down into the vertebral canal
  • can be silent of symtomatic with symptoms arising due to impaired csf flow/medullary compression
32
Q

Joubert syndrome:

  • hypoplasia of ___
  • sign on imaging
  • mutations that encode what?
A

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

  • gives rise to the molar tooth sign on imaging
  • mutations that encode components of the primary cilium
33
Q

Dandy-walker

  • deformations present
  • cyst where?
  • what condition is often present
A

enlarged posterior fossa, cerebellar vermis absent or barely present

  • midline cyst that is lined by ependymal cells and is contiguous with leptominges on its outer surface
  • the cyst represents the roof of the expanded 4th ventricle
  • dysplasias of the brainstem nuclei are commonly associated
34
Q

Syringomyelia:

  • formation of a fluid filled cavity where?
  • associated with?
  • symptoms?
  • onset age?
A
  • formation of ff cavity in the inner portion of the cord (syrinx) that can extend into the brainstem (syringobulbia)
  • associated with arnold chiari, intraspinal tumors, or follwoing traumatic injury
  • results in destruction of the adjacent neural tissue that is surrounded by reactive gliosis–> cape like bilateral loss of pain/ temp sensation in UE’s, still have fine touch pressure

-onset is 2nd-3rd decade of life, except trauma

35
Q

Hydromelia

A

expansion of the ependymal lined cord of the central canal of the cord

-destruction of the adjacent neural tissue that is surrounded by reactive gliosis

36
Q

Perinatal BI: Cerebral palsy

  • progression
  • characteristics
  • when is insult
A
  • non progessive neurologic deficit characterized by combinations of spasticity, dystonia, ataxia/athetosis, and paresis
  • due to insults that occur in the prenatal and perinatal periods
37
Q

Perinatal BI: parenchymal hemorhage

  • whos at risk
  • where does it occur?
  • what can it lead to?
A
  • premature infants are more at risk
  • occurs within the germinal matrix near the jxn between the developing thalamus and caudate nucleus
  • can lead to hydrocephalus
38
Q

Perinatal BI: Periventricular leukomalacia:

  • who is at risk
  • occurs where?
  • what is the apperance
A
  • premis have greater risk
  • occur in the supratentorial periventricular white matter
  • take the form of chalky yellow plaques consisting of discrete regions of white matter necrosis and calcification
39
Q

Perinatal BI: Multicystic encephalopathy:

-what is damaged?

A

infarcts can cause damage to both grey and white matter leading to large destructive cysts

40
Q

Symptoms of perinatal ischemic lesions of the cerebral cortex

  • gyri?
  • status marmoratus?
A
  • thinned out gliotic gyri (ulegyria)
  • damaged basal ganglia and thalamus can occur w/ patchy neuronal loss and reactive gliosis
  • later there can be abnormal myelization that gives rise to a marble like appearance of the deep nuclei (status marmoratus)
41
Q

distatic fxs

A

cross sutures of the skull

42
Q

direct parenchymal injury:

  • what part of brain most at risk
  • most common sites
  • coup vs contrecoup
A

contusions, lacerations

  • direct force greatest on the crests of the gyri
  • most common at frontal lobes along the orbital ridges and the temporal lobes
  • coup is side of contact (immobile head), contrecoup is site opposite of contact. (mobile head has both)
43
Q

diffuse axonal injury:

  • microsocpic findings
  • injury caused by
  • swelling best demonstrated by which staining technique
  • what is seen later
A

deep white matter regions (Corpus callosum, paraventricular, and hippocampal areas in the supratentorial compartment), cerebral peduncles, superior colliculi, deep reticular formation

  • microscopic findings: axonal swelling, focal hemorrhagic lesions
  • injury due to direct action of mechanical forces with subsequent alterations in axoplasmic flow
  • silver impregnation techniques or w/ immunoperoxidase stains for axonally transported proteins such as app and a synuclein
  • later, increased numbers of microglia are seen in damaged areas, there is subsequent degeneration of the involved fiber tracts
44
Q

Morphology of a brain contusion:

  • early
  • next few hours
  • after about a day
  • old
A

early: edema and hemorrhage that is PERIcapillary

Next few hours: blood leaks out throughout the rest of the surrounding tissue

After about a day: pyknosis of the nucleus, eosinophilia of cytoplasm, and disintegration of the cell

old: depressed, retracted, yellow-brown, can later become foci for epileptic attacks, eventually gliosis and hemosiderin laden Mfs predominate

45
Q

Epidural hematoma:

  • occurs how?
  • symtoms?
A

occurs when an artery like the mma that lies between the fused dura and periosteum ruptures

-the pt is lucid for the first several hours but then declines as the pressure increases

46
Q

subdural hematoma:

  • how does it occur
  • common in who
A

occurs when the bridging veins in the subdural space rupture. more common in old people with brain atrophy and infants due to their thin walled veins

47
Q

know this table

A
48
Q

Morphology of acute subdural hematoma:

  • gross appearance
  • when does lysis of the clot occur
  • when does growth of fibroblasts from dural surface into hematoma occur
  • when does early development of hyalinized cxn tissue occur
A
  • appears as a collection of freshly clotted blood along the brain surface without extension into the depths of sulci. the underlying brain is flattened and the subarachnoid space is often clear.
  • lysis: 1 week
  • fibroblasts: 2 weeks
  • hyalinized cxn: 1-3 months
49
Q

symtoms of subdural hematoma:

  • timing
  • most common where
  • signs
A

manifest within 48 hours, often nonlocalizing such as headache and confusion, slowly progressive is typical, but fast decomp can occur

50
Q

posttraumaitc hydro

A

due to obstruction of CSF resorption from the hemmorhage into the subarachnoid spaces

51
Q

CTE gross presentation

-protein tangles of ? where?

A

brains are atrophic, enlarge ventricles, increased amounts of tau-containing neurofibrilary tangels that invole the superficial frontal and temproal lobes

52
Q

morphology of spinal cord injuries

-above and below site

A

the central areas become cystic and gliotic and the areas above and below the injury show wallerian degeneration involving the long white matter tracts

53
Q

Global cerebral ischemia:

  • occurs due to what kind of events?
  • sensitivity of brain tissue
A

-oc

NS2 Exam 2 (2 decks)

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