Neuropathology Part 1 (8) Flashcards
acute vs chronic reactions to neurons to injury overall
acute- often anaerobic or glucose depleted in neurocytes
chronic- accumulation of abnormal pros
what is an accumulation of misfold pros called
proteinopathies
actute neuronal injury- why, what do they look like histologically
- 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
axonal rxn to injury and how does it look
- 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
What is the most impprtant morpholohical indicator of CNS injury
Gliosis
what is the reaction of microglia to injury (4)
- proliferation
- developing elongated nuclei (neurosyphylis)
- Forming aggregates around small foci of necrotic tissues
- congregating around cell bodies of dying neurons
What is vasogenic edema
increased extracellular fluid caused by bb disruption and increased vascular permeability (shift from intravascuar compartment to intracellular spaces)
What is cytotoxic edema
increase in intracellular secondary to neuronal, glial or endothelial cell membrane damage
What does hydrocephalous cause
brain atrophy
increase in lat ventricles
what is primary vs secondary neurotrauma
primary damage- focal lesions and diffuse axonal injury
Secondary damage- intracranial hematomas, edema, intracranial herniation, infarction, inderction
3 main types of missile injury to brain
- depressed- just causes depressed skull fx w/ contusion
- Penetrating- enters but doesn’t exit
- Perforating- missile enters and extits
what is a displaced vs diastatic fx
displaced- bone displaced into cranial cavity
distatic- fx crosses sutures
what is the mc parenchymal injury
concussion clinical syndrome of altered consciousness seconday to head injury
extradural intracranial hemorrhage- mech and clinical manisfication
skull fx w arterial blood (middle meningeal aa)
-lucid interval followed by a rapid increase in intracranial pressure
Subdural hematoma mech and clinical manisfication
bw dura and arachnoid- rupture of venus sinuses or small bridging veins
-acute presentation with rapid increase in intracranial prssure