Neuropathology Part 1 (8) Flashcards

1
Q

acute vs chronic reactions to neurons to injury overall

A

acute- often anaerobic or glucose depleted in neurocytes

chronic- accumulation of abnormal pros

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2
Q

what is an accumulation of misfold pros called

A

proteinopathies

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3
Q

actute neuronal injury- why, what do they look like histologically

A
  • changes that accompany acute CNS hypoxia/ischemia
  • reflect the earliest morphological markers of neuronal cell death
  • red neurons are evident by 12-24 hrs after insult
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4
Q

axonal rxn to injury and how does it look

A
  • observed in the celly body during regeneration of axon (best seen in ant horn)
  • enlargement and rounding of cell body, peripheral displacement of nucleus, enlargement of nucleolus
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5
Q

What is the most impprtant morpholohical indicator of CNS injury

A

Gliosis

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6
Q

what is the reaction of microglia to injury (4)

A
  • proliferation
  • developing elongated nuclei (neurosyphylis)
  • Forming aggregates around small foci of necrotic tissues
  • congregating around cell bodies of dying neurons
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7
Q

What is vasogenic edema

A

increased extracellular fluid caused by bb disruption and increased vascular permeability (shift from intravascuar compartment to intracellular spaces)

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8
Q

What is cytotoxic edema

A

increase in intracellular secondary to neuronal, glial or endothelial cell membrane damage

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9
Q

What does hydrocephalous cause

A

brain atrophy

increase in lat ventricles

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10
Q

what is primary vs secondary neurotrauma

A

primary damage- focal lesions and diffuse axonal injury

Secondary damage- intracranial hematomas, edema, intracranial herniation, infarction, inderction

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11
Q

3 main types of missile injury to brain

A
  1. depressed- just causes depressed skull fx w/ contusion
  2. Penetrating- enters but doesn’t exit
  3. Perforating- missile enters and extits
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12
Q

what is a displaced vs diastatic fx

A

displaced- bone displaced into cranial cavity

distatic- fx crosses sutures

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13
Q

what is the mc parenchymal injury

A

concussion clinical syndrome of altered consciousness seconday to head injury

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14
Q

extradural intracranial hemorrhage- mech and clinical manisfication

A

skull fx w arterial blood (middle meningeal aa)

-lucid interval followed by a rapid increase in intracranial pressure

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15
Q

Subdural hematoma mech and clinical manisfication

A

bw dura and arachnoid- rupture of venus sinuses or small bridging veins

-acute presentation with rapid increase in intracranial prssure

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16
Q

Subarachnoid space hemorracge mechanism, clinical

A

arterial rupture

-Manigeal irratation w a rapid increase in intracranial pressure (worst headache ever)