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Maddy - NMSP Exam II > Path - Intro to Neuro > Flashcards

Path - Intro to Neuro Flashcards

1
Q

what is central chromatolysis

A

nissl removed from the center of the cell to the periphery

  • seen in the axonal reaction
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2
Q

intranuclear inclusions should make you think of what conditions

A

herpes or CMV

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3
Q

intracytoplasmic inclusions should make you think of what conditions

A
  • rabies
  • alzheimer’s
  • parkinson
  • CJD (Creutzfeldt–Jakob disease)
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4
Q

intracytoplasmic neurofibrillary tangles indicate _____

A

alzheimer’s

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5
Q

intracytoplasmic negri bodies indicate _____

A

rabies

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6
Q

in what conditions are Alzheimer’s type 2 astrocytes seen

A

not associated with Alzheimer’s just the same doc named them

  • hyperammononemia (chronic liver dz)
  • wilson dz
  • hereditary metabolic disorder of the urea cycle
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7
Q

what is astrogliosis

A

an abnormal increase in the number of astrocytes due to the destruction of nearby neurons

  • a reaction to craniopharyngioma (tumor from rathke pouch)
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8
Q

histologic hallmark of astrogliosis

A

Rosenthal fibers

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9
Q

in what conditions are Rosenthal fibers seen

A
  • reaction to craniopharyngioma (tumor)
  • long standing gliosis (pilocytic astrocytoma)
  • Alexander disease
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10
Q

describe morphology of Rosenthal fibers

A

thick, elongated, brightly eosinophilic, irregular structures occurring within astrocyte processes

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11
Q

PAS+ stain should indicate ____

A

corpora amylacea

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12
Q

what is corpora amylacea

A

aging process of cells

  • increase with age
  • represents degenerative change
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13
Q

concentrically laminated, layered onion-looking histological marker indicates ____

A

corpora amylacea

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14
Q

CR3 and CD68 markers indicate what cells

A

microglia (macrophages of the CNS)

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15
Q

what is neuronophagia

A

the destruction of nerve cells by phagocytes

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16
Q

what is progressive multifocal leukoencephalopathy

A

a progressive demyelinating and usually fatal disease caused by the JC virus that destroys oligodendrocytes in the brain

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17
Q

what is multiple system atrophy

A

a fatal neurodegenerative disorder characterized by the abnormal accumulation of toxic forms of the synaptic protein alpha-synuclein (α-syn) within oligodendrocytes and neurons

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18
Q

compare vasogenic and cytotoxic edema

A

vasogenic: increase in EXTRAcellular fluid
cytotoxic: increase in INTRAcellular fluid

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19
Q

what are the pathological causes of hydrocephalus

A
  • increased production of CSF
  • obstruction
  • decreased absorption of CSF (outflow obstruction)
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20
Q

what occurs in response to increased CSF

A
  • absorption
  • dilation of frontal and temporal horns
  • elevation of corpus callosum
  • thinning of the cerebral mantle
  • stretching/perforation of the septum pellucidum
  • enlargement downward of third ventricle
  • papilledema
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21
Q

what can cause increased CSF production?

A

choroid plexus papilloma

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22
Q

appearance of broccoli (thick fibrous core/stalk) on histo indicates ____

A

choroid plexus papilloma

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23
Q

describe pyogenic meningitis

A

suppurative exudate covering the brainstem and cerebellum –> obstructive hydrocephalus

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24
Q

causes of acquired hydrocephalus

A
  • infections (meningitis)
  • mass lesions (neoplasms)
  • inflammation
  • post-hemorrhage
  • choroid plexus papilloma
  • sagittal sinus thrombosus
  • hypervitaminosis A
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25
Q

too much vitamin A can lead to what brain condition

A

acquired hydrocephalus

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26
Q

why is the CSF normal in hydrocephalus ex-vacuo?

A

because it is a slow process - has time to normalize

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27
Q

the clinical triad of urinary incontinence, gait disturbance, and dementia, indicate what dz process?

“wet, wacky, and wobbly)

A

normal pressure hydrocephalus

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28
Q

effects of tonsillar herniation

A

respiratory and cardiac center compression

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29
Q

describe kernohan’s notch phenomena

A

compressor of the cerebellar peduncle against the tentorium cerebella due to a transtentorial herniation

–> canes ipsilateral hemiparesis or hemiplegia on the side of the herniation

produces a visible “notch” in cerebellar peduncle

30
Q

compare hypoxia and ischemia

A

hypoxia: low partial pressure of O2
ischemia: impairment of blood’s oxygen carrying capacity, or inhibition of O2 usage

31
Q

what signs does the Sommer sector of the hippocampus show in hypoxia

A

shows decreased number of cells

32
Q

what areas of the brain are first to show signs of hypoxia

A

purkinje of the cerebellum

pyramidal cells of the Sommer’s sector of the hippocampus (areas CA1 and CA2)

33
Q

what signs does the purkinje of the cerebellum show in hypoxia

A

shrunken, eosinophilic, pyknotic cells

“dead red guys”

34
Q

compare liquefactive and coagulative necrosis

A

liquefactive: no architectural remnants
coagulative: there are architecture remnants

35
Q

histological hallmark of cerebral infarction

A

missing neuropil, appears pale, decreased number of cells

36
Q

what is a hygroma

A

separation of arachnoid from the dura due to contraction of underlying brain parenchyma s/p infarct

37
Q

describe myelomeningocele

A

extension of the CNS tissue through a defect in the vertebral column (most often lumbosacral)

38
Q

describe meningocele

A

protrusion of the meninges through a defect in the vertebral column

39
Q

describe encephalocele

A

disorganized brain tissue extending through defect in cranium (usually posterior fossa)

40
Q

describe anencephaly

A

absence of most of the brain and calvarium, but still have cerebellum and brainstem

41
Q

in what trimester do encephaloceles and ancecenphaly occur

A

first trimester

42
Q

in what trimester do lissencephalia and microgyria occur

A

second semester

43
Q

fetal alcohol syndrome, HIV-1, and Zika virus can cause what forebrain anomalies

A

microcephaly

44
Q

describe lissencephaly

A

decreased number of gyro with a smooth or “cobblestone” surface

45
Q

describe polymicrogyria

A

small, unusually numerous, irregularly formed convulsions of the gyri

46
Q

describe neuronal heterotopias

what condition are they associated with

A

collections of neurons in inappropriate places along the pathway of migration

associated with epilepsy

47
Q

describe holoprosencephaly and how it presents clinically

A

incomplete separation of the cerebral hemispheres across the midline

clinical: cyclopia, arrhinenceophaly

48
Q

what is arrhinenceophaly

A

absence of olfactory cranial nerves

49
Q

describe dandy walker malformation

A

enlarged posterior fossa with expanded, roofless fourth ventricle
- cerebellar vermis is absent and replaced by a cyst

50
Q

describe Joubert syndrome

A

hypoplasia of the vermis, elongation of cerebellar peduncles and altered brainstem shape

“molar tooth sign”

51
Q

molar tooth sign is indicative of _____

A

jobbery syndrome

52
Q

describe syringomyelia and its sx

A

a fluid filled cleft-like cavity in the inner portion of the spinal cord

sx: isolated loss of pain and temp sensation of upper extremities bilaterally

53
Q

describe hydromyelia

A

expansion of the ependymal-lined central canal of the cord

54
Q

where are intraparenchymal hemorrhages seen

A

in germinal matrix

55
Q

chalky yellow plaques are indicative of what dz process

A

periventricular leukomalacia

56
Q

compare where skull fractures usually occur in an awake patient and in an LOC patient

A

awake: usually fall backward –> occipital fx

LOC: usually fall forward –> frontal impact

57
Q

sx of basal skull fracture

A

otorrhea/rhinorrhea from CSF drainage from ear or nose

58
Q

describe a TBI/CTE

A

some level of damage to the brain from an external mechanical force

  • associated diminished or altered state of consciousness
  • brain function temporarily or permanently impaired
59
Q

when can CTE (chronic traumatic encephalopathy) be diagnosed?

A

only when examining brains after death

60
Q

morphology of CTE (chronic traumatic encephalopathy)

A

progressive loss of normal brain matter and an abnormal buildup of the protein tau

61
Q

hyperphosphorylated tau protein as neurofibrillary tangles, astrocytic tangled, and neuritis in striking clusters around small blood vessels of the cortex indicates what dz process

A

chronic traumatic encephalopathy (CTE)

62
Q

general features of CTE

A
  • neurofibrillary tangles/amyloid and tau deposition
  • depigmentation of substantia nigra
  • cerebral atrophy/enlarged ventricles
  • micro-hemorrhages/DAD
63
Q

what would cause a contrecoup parenchymal in jury of the brain

A

sudden deceleration –> head going forward, so brain hits the skull on the back

the brain contacts the skull on the side opposite from where impact occurs

64
Q

yellowish brown patches involving the crests of the gyro indicate what

A

plaque jaune

- old trauma lesions

65
Q

what is diffuse axonal injury

A

axonal swelling and/or focal hemorrhagic lesions that appear within hours

66
Q

morphology of diffuse axonal injury

A

increased number of microglial areas and degeneration of involved tracts

67
Q

axonal spheroids indicate what dz process

A

diffuse axonal injury

68
Q

what microscopic test should be performed to diagnose shaken impact syndrome

A

microscopic iron to identify old bleeding

- use a Prussian blue stain

69
Q

trauma in the epidermal space occurs how, what sx, and what type of blood is involved

A

how: skull fracture
sx: rapidly evolving neurologic sx
blood: arterial

70
Q

trauma in the subdural space occurs how, what sx, and what type of blood is involved

A

how: mild trauma
sx: slowly evolving neurologic sx
blood: venous

Maddy - NMSP Exam II (12 decks)

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