Intro into NeuroPathology Flashcards

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1
Q

Describe the Acute Response to Neuronal Injury. When would you see it? What would you see?

A
12-24 hrs
Red Neurons
Shrinkage of cell body
Pyknosis
Intense eosinophilia of cytoplasm
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2
Q

In what conditions will acute injury occur?

A

Hypoxia
Hypoglycemia
Trauma

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3
Q

What would you see with a Subacute and Chronic Response to neuronal injury?

In what conditions, would you see this occur?

A

Degeneration; progressive
Cell loss and reactive gliosis; Apoptosis

Neurodegenerative dz or demyelinating dz

  • Abnormal protein accumulation
  • ALS
  • Alzheimer’s
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4
Q

How do axons react to neuronal injury?

A

Increase protein synthesis with axonal sprouting

Enlarged cell body
Central chromatolysis = nissl substance to periphery (also nucleus)

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5
Q

What are some intracytoplasmic inclusions?

A

Lipofuscin (increases with age)
Negri bodies - Rabies
Neurofibrillary tangles - ALZ
Lewy bodies - Parkinson

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6
Q

What are some intranuclear inclusions?

A

Cowdry bodies - Herpes

CMV = intranuc and intracyt

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7
Q

What is histologically characteristic of CMV infection?

A

Owl’s eye nuclear inclusions

damages ependymal cells

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8
Q

What is the most important histopathologic indicator of CNS injury?

A

Astrogliosis!

Regardless of etiology

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9
Q

Describe Alz Type 2 astrocytes. When would you see them?

A

Gray matter cell
Large nucleus
Pale staining central chromatin
Intranuclear glycogen droplet

Hyperammononemia (chronic lever dz)
Wilson Dz
Hereditary metabolic DO of urea cycle

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10
Q

What cancer would you associate astrogliosis with? What other characteristics can be seen?

A

Craniopharyngioma

Rosenthal fibers
Keratin
Cystic tumor
Drainage like machine oil

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11
Q

When would you see rosenthal fibers? What do they contain?

A

During a slow and benign process
At areas of long standing gliosis = Pilocytic astrocytoma

Contains 2 heat shock proteins = a-B-crystalline,HSP27
Ubiquitin

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12
Q

What characteristics would you see with Corpora Amylacea?

A

Polyglucosan bodies
PAS+
Increase with age
Degenerative change

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13
Q

What are the macrophages of the CNS? What are the surface markers? How do they respond to injury?

A

Microglia
CR3 and CD68

Respond by:
Proliferating
Microglial nodules - aggregate around necrosis
Neuronophagia - congregate around cell bodies of dying neurons

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14
Q

What injuries do oligodendrocytes respond to? Name specific dz and what you see.

A

Demyelinating DOs, Leukodystrophies

PML = intranuclear inclusions
MSA (multiple system atrophy) = glial cytoplasmic inclusions (a-synuclein)

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15
Q

Where do you see a-synuclein?

A

Parkinson’s
Lewy Body dementia
MSA
Diffuse axonal injury (DAI)

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16
Q

Describe ependymal cells. What are ependymal granulations?

A

Line ventricles, ciliated columnar cells

Granulations = disruption of ependymal lining and proliferation of subependymal astrocytes

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17
Q

Describe vasogenic edema. What does it often follow?

A

Increase in extracellular fluid due to BBB disruption and increased vascular permeability

Follows ischemic injury
No lymphatics to clear fluid away

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18
Q

Describe cytotoxic edema.

A

Increase in intracellular fluid secondary to neuronal, glial, or endothelial cell membrane injury

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19
Q

Which type of edema would you see more? What can it lead to?

A

Often see elements of BOTH vasogenic and cytotoxic edema = gyri flatten, sulci narrow, ventricles compressed –> HERNIATION

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20
Q

What is the one bacterial dz that will affect the bottom of the brain? What pathology will it lead to?

A

Pyogenic meningitis = suppurative exudate covering brainstem and cerebellum

Thickened leptomeninges –> obstructive hydrocephalus

21
Q

Wet, Wobbly, Wacky?

A

Gait disturbance, Dementia, Urinary incontinence

Seen with NPH

22
Q

What are the different types of herniation? What conditions will they cause?

A

Subfalcine = cingulate gyrus under the Falx

Transtentorial = medial aspect of the temporal lobe compressed against tentorium
CN3 –> dilated pupil and impaired eye movement

Tonsillar = cerebellar tonsils through foramen magnum –> respiratory and cardiac compression

23
Q

What is the Kernohan’s notch phenomenon? What does it cause?

A

Compression of CEREBRAL peduncle against tentorium cerebelli

Due to Transtentorial herniation

Ipsilateral hemiparesis or hemiplegia (on side of herniation) –> a RIGHT hemisphere herniation causes LEFT notch leading to RIGHT-sided motor impairment

24
Q

What is Duret hemorrhage?

A

Progression of transtentorial herniation –> secondary hemorrhagic lesions in midbrain and pons

25
Q

Describe liquifactive necrosis. What can cause this?

A

Digestion of tissue into liquid viscous mass, no architectural remnants

Bacterial infections
CNS Infarct

26
Q

All other organs (except the brain) undergo this type of necrosis.

A

Coagulative Necrosis (architecture remains)

27
Q

What is a hygroma?

A

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

28
Q

What accounts for the most CNS malformations? Describe it. What might be one reason that it is so common?

A

Neural Tube Defects

failure of portion of neural tube to close or reopening after closure

Folate deficiency = neural tube closure by 28 days before pregnancy is recognized

29
Q

What is an encephalocele?

A

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

30
Q

Which defects will you see in the 1st trimester? 2nd trimester? 3rd trimester?

A

1st = encephalocele, anencephaly

2nd = Lissencephalia, Microgyria

3rd = myelinating issues

31
Q

B/w megalocephaly and microcephaly, which is more common? What can cause this?

A

Microcephaly - decreased number on neurons in neocortex

Usually assoc with small head circumference
Chromosomal abnormalities
Fetal Alcohol Syndrome 
HIV-1 in utero 
Zika virus
32
Q

What is neuronal heterotopia? What is it commonly associated with?
What genes are responsible?

A

Collections of neurons in inappropriate places

Associated with epilepsy

X-chromosome –> Filamin A protein and DCX = Lissencephaly in males and heterotopia in females

33
Q

What is holoprosencephaly? Associations? Genes?

A

Incomplete separation of cerebral hemispheres across midline

Assoc with cyclopia, arrhinenceophaly (absence of CN 1)

Trisomy 13, SHH

34
Q

What is polymicrogyria?

A

Small, unusually numerous, irregularly formed convolutions

Entrapment of meningeal tissue

35
Q

What do you see with agenesis of the corpus callosum?

A

Bat-wing lateral ventricles

Mental retardation or normal mentation

36
Q

Which is more serious Chiari Type 1 or 2? Describe them. What are their associations?

A

Small posterior fossa with Type 2 being more serious

Type 2 = misshapen midline cerebellum with vermis through F magnum
-Assoc = hydrocephalus, myelomeningocele

Type 1 = Tonsils through FM, Silent, Sx if impaired CSF flow
-Assoc = syringomyelia

37
Q

What is a Dandy-Walker malformation? Characteristics?

A

Enlarged posterior fossa

Expanded roofless 4th ventricle

Vermis absent/rudimentary

Cyst with ependymal lining contiguous with leptomeninges on outer surface

38
Q

What is Joubert syndrome?

A

Hypoplasia of vermis

Elongation of cerebellar peduncles and altered brainstem

Molar tooth sign

39
Q

What is syringomyelia?

A

Fluid filled cavity in the inner portion of spinal cord

B/L loss of Pain and Temp of UE
-Interrupts fibers that cross through anterior white commissure

40
Q

What is Hydromyelia?

A

Expansion of ependymal-lined central canal of cord

41
Q

Decribe characteristics of cerebral palsy.

A

Spasticity
Dystonia
Ataxia/Athetosis
Paresis

42
Q

Name the perinatal brain injuries. What might you see with them?

A

Cerebral palsy

Intraparenchymal hemorrhage

Periventricular leukomalacia (chalky yellow plaques)

Multicystic encephalopathy (large destructive cystic lesions)

Ulegyria (thinned gyri from ischemic lesions)

43
Q

What is a diastatic fracture?

A

Crosses a suture

44
Q

What are the sign of a basilar skull fracture?

A

Hemotympanum
Battle’s sign - bruising behind ear
Racoon eyes
Otorrhea/Rhinorrhea = CSF drainage form ear/nose

45
Q

Describe a Traumatic Brain Injury (TBI).

A

Brain damage form external mechanical forces (rapid acceleration, impact, etc)

Associated diminished or altered state of consciousness, brain function temp/perm impaired

46
Q

How would you diagnose CTE? How do you get it? What happens?

A

DX only after examining brain after death

Get it from repeated head blows 
Progressive loss of normal brain matter and abnormal build up of Tau 
Microhemorrhages/DAD
NF tangles/amyloid - 43% 
Depigmentation of substantia nigra
47
Q

What is Plaque Jaune?

A

Depresses, retracted, yellowish brown patches involving crest of gyri

Contusion - countercoup

Old trauma lesions
Temporal and occipital lesions

48
Q

What is Diffuse Axonal Injury? What stains? Histologically significant?

A

Axonal swelling +/- focal hemorrhagic lesions (within hours) from mechanical forces

Silver stain or APP/a-synuclein immunostains

Axonal spheroids

49
Q

Etiology of: epidural, subdural, SAH.

A

Epidural = trauma to Middle meningeal (dura peeled off)

Subdural = trauma affecting venous system

SAH = vascular/trauma, sudden onset of severe HA