Lecture 3 Intro to Neuropath Flashcards

1
Q

what is the pathway of flow of the CSF

A

CSF is produced in the choroid plexus–> lateral ventricles–> foramen of Monro–> 3rd ventricle–> aqueduct of Sylvius–> 4th ventricle–> foramen of luschka and Magendie–> subarachnoid space–> reabsorbed in the arachnoid granulations.

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2
Q

What are the neuroectoderm-derived cells of the CNS

A

Neurons, and glial cells(support neurons) which contain Astrocytes, oligodendrocytes, and ependymal cells

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3
Q

What are the mesoderm derived cells of the CNS

A

Microglial cells (“police of the brain”) and endothelial cells

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4
Q

The cerebral cortex gray matter has how many layers and with what surface

A

the cerebral cortex gray matter has 6 layers. Layer 1(molecular layer) contains the pial surface. White matter lies underneath layer 6. Gray matter contains mostly neuronal cell bodies and glial cells.`

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5
Q

The hippocampus is important for what function

A

short-term memory; there are only 3 layers in this area of the brain. The dentate gyrus is located in the middle of the hippocampus.

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6
Q

which area of the hippocampus is more susceptible to damage under different stresses

A

CA1 is the most susceptible to hypoxic damage.

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7
Q

What pathologic changes do you get with ischemia, degenerative diseases, neuro-degenertation, neurons undergoing single cell death?

A
  • acute eosinophilic change (pink) due to ischemia
  • central chromatolysis leads to cytoplasm swells if a neuron has its axon damaged
  • simple atrophy in degenerative diseases
  • neuro-degeneration seen in Alzheimer’s you will see neurofibrillary change
  • neurons undergoing single cell death the neurons will show apoptosis
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8
Q

what is the function of astrocytes?

A
  • support neurons by supplying nutrients
  • component of the blood brain barrier
  • Contribute to the glia limitans of the brain-CSF barrier (pia mater)
  • recycle neurotransmitters
  • Contain intermediate filaments (composed of glial fibrillary acidic protein GFAP)
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9
Q

How do astrocytes function in reactive astrocytosis?

A
  • React to changes in the brain with gliosis and help brain healing by becoming hypertrophic (gemistocytes). In chronic conditions, the gemistocytes may progress to fibrillary astrocytes (aka fibrillary gliosis)
  • When exposed to hyperammonemia, they become “Alzheimer’s type 2 astrocytes” (empty nuclei)
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10
Q

Histologically you can see astrocytes where during reactive astrocytosis?

A

they can be seen with dense pink cytoplasm and thick processes. At the edge of a brain infarct, you will see many astrocytes undergoing reactive astrocytosis

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11
Q

what are the characteristics of oligodendrocytes

A
  • Produce and maintain myelin in the CNS
  • One oligodendrocyte myelinates up to 50 neuronal processes
  • Smaller than astrocytes, round nuclei, clear cytoplasm (with fried egg appearance)
  • Luxol fast blue H&E stain–> myelin stain
  • Most oligodendrocytes are in the white matter (where the axons are too)
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12
Q

What are the characteristics of microglial cells

A
  • mesoderm-derived
  • small elongated cells in both gray and white matter
  • antigen-presenting cells
  • Can become phagocytes (and turn into lipid-laden macrophages aka gitter cells
  • Iba- 1 stain marks microglial cells
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13
Q

How do microglial cells function in the face of viral encephalitis?

A

In viral encephalitis, microglial cells can participate in neuronophagia (attempt at killing infected neuron) and form microglial nodules (bunch of microglial cells coming together in an area of neuronophagia).
These microglial cells become round looking phagocytes full of hemosiderin and lysed RBCs.

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14
Q

What marks lipid-laden macrophages that came from microglial cells

A

Oil red O stain

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15
Q

List the selective vulnerability of neurons to hypoxia?

A
  • most susceptible: Pyramidal neurons of CA1 (sommer’s sector)
  • Also highly susceptible: Purkinje cells of the cerebellum
  • Also susceptible: Pyramidal neurons in middle layers (III, IV, V) of cerebral cortex, neurons in basal ganglia

-Relatively resistant: Neurons in brainstem and spinal cord

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16
Q

what are the pathological changes due to ischemia

A
  • hypereosinophilic
  • shrinking of nucleus and less detailed
  • nucleoli will be harder to find
17
Q

what are the 3 components of the blood-brain barrier?

A
  • Capillary endothelial cells (endothelial cells have tight junctions, fewer pinocytic vesicles, and many mitochondria)
  • Basement membrane
  • Astrocyte foot processes (Can see the astrocytes sending down foot processes to surround the vessels)
18
Q

Vasogenic edema of the brain is due to what and causes

A

disruption of the BBB (by infarct, tumor, hemorrhage, etc)…cause increased intracranial pressure, which may lead to herniation.

19
Q

What is contrast enhancement?

A

Normally, imaging contrast should not penetrate the brain, but if there is a neoplasm in the brain, it can penetrate and you can see it radiographically. The abnormal vessel BBB leads to edema and contrast enhancement.

20
Q

what are the different types of herniation?

A
  • Transtentorial

- Tonsillar

21
Q

what are the three types of transtentorial herniation?

A
  • Uncal (unilateral, most common)
  • Central
  • Rostro-caudal deterioation
22
Q

When the supratentorial structures push the brain stem down, the vessels can tear and cause hemorrhage. This is called?

A
  • Duret hemorrhage of the brainstem

- This is either caused by uncal or central herniation

23
Q

what are the characteristics of central herniation?

A

-edematous brain(tight sulci) and an infarcted middle cerebral artery (MCA) area. The brain has been pushed down due to the edema, so you can see bowing of the corpus callosum, Duret hemorrhages in the brainstem, and pushed down hippocampi

24
Q

What are the characteristics of tonsillar herniation

A

-occurs when the cerebellar tonsils increase in either mass or volume.
tonsils are pushing down through the foramen magnum to surround the medulla

25
Q

what are the types of hydrocephalus?

A
  • Non-communicating (AKA internal AKA obstructive) due to an obstruction in the flow of CSF(commonly in the aqueduct of sylvius
  • Comunicating (AKA External) due to accumulation of CSF due to problem with CSF reabsorption
  • Congenital: most common form is stenosis of the aqueduct which can be due to
    1. Congenital stenosis of the aqueduct or 2. Post-infectious aqueduct stenosis (CMV infection from mom)
26
Q

Epidural Hematoma

A
  • Between dura mater and the skull
  • Fracture of temporal bone–> tear of middle meningeal artery
  • Arterial bleeding, therefore blood accumulates rapidly
  • Lucid interval after the trauma, followed by coma in a few hour, progressing eventually to uncal transtentorial herniation
  • lentiform shape on CT scan
  • Treatment: Drain the hematoma ASAP to decrease ICP
27
Q

Subdural Hematoma

A
  • Due to tear of bridging veins between brain and venous sinuses
  • Prone to occur in brains with atrophy (stretches bridging veins)
  • Can be seen in Alzheimer’s patient and symptoms may mimic dementia
  • Venous bleeding, so blood accumulates slowly
  • Can become chronic with organization
28
Q

Cerebral contusions

A
  • associated with rapid impact of the inferior frontal and temporal lobes against the irregular surfaces of the anterior and middle cranial fossae
  • Contre-coup: injury occurs on the opposite side of where the impact was
  • Hemorrhagic infarction of the crowns of the gyri (surface lesions)
29
Q

diffuse axonal injury (DAI)

A
  • associated with high impact injury (ex high speed MVA)
  • patients usually present in a coma (severe injury)
  • axons in white matter experience shearing forces and tear
  • axons tear and curl up into “axonal spheroids”
  • can be seen in “shaken baby syndrome”
30
Q

Spinal Cord trauma

A
  • often seen after MVA, horse riding accidents, diving accidents, sports-related injuries, knife or firearm assaults
  • shaken baby syndrome can also cause cervical or cervicomedullary spinal cord trauma