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Flashcards in Cerebral Vascular Diseases Deck (45)
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What are astrocytes and what is their function?

They are cells responsible for repair and scar formation in the brain. They are found in both the gray and white matter, with round/oval nuclei and pale chromatin.


What is scar formation called in the CNS?

Gliosis, not fibrosis.


What are "oligodendrocytes?"

They form myelin; they myelinate many internodes in CNS and have small round lymphocyte like nucleus.


What are "Ependymal cells"?

Cells responsible for forming the CSF, thus they line the ventricles.


What are "Microglia"? What is their CD marker? What do they look like?

The monocyte/macrophage equivilent in the CNS. CD68 +. Elongated, weird shaped nucleus with clumped nucleolus.


What are "microglial nodules" and "neuronophagia?"

Microglial nodules is the term given to the structure formed when the microglial cells aggregate around a small foci of tissue necrosis, whereas a neuronophagia is congregation of microglia around neuronal cell bodies of dying neurons.


What are "Red Neurons?"

The type of neurons we can see in acute neuronal injury, in response to acute CNS hypoxia/ischemia and this eventually leads to cell death.


What do we see histologically in subacute or chronic neuronal diseases?

Cell loss and reactive gliosis.


Describe the process of "Gliosis"

It is the CNS response to injury, the equivilent to fibrosis in which the astrocytes undergo changes.


What is "Gemitocytic Astrocytes?"

These are hypertrophic and hyperplastic astroyctes with pink cytoplasm and stout ramifying processes, and we see them during the process of gliosis.


What is "Global Cerebral Ischemia?"

Diffuse hypoxia/ischemic encephalopathy. Idea is, in response to something like an MI the whole brain ends up being hypoperfused and leads to a global ischemia in the entire brain. Shock can also cause this.


Which cells in the brain are most sensitive to oxygen depletion?



Histologically how does the brain present after a global cerebral ischemia episode?

Edematous brain with wide gyri and narrow sulci; cut surfaces show poor demarcation between the gray and white matter.


12-24 hours after global cerebral ischemia, what can we expect to see? What kind of infiltrates do we see?

The "red neurons," microvacuolization, nuclear pyknosis (where the nucleus becomes small and dark) followed by karryorhexis and then eventually lysis. Also see neutrophil infiltrates.


What kind of necrosis do we see in the brain?

Liquifactive necrosis.


What do we see 24 hrs to 2 weeks after Global cerebral ischemia? What kind of infiltrates?

Subacute changes, necrosis of tissues, influx of macrophages, vascular proliferation and reactive gliosis.


What happens after 2 weeks following global cerebral ischemia?

Repair, removal of necrotic tissue and as a result alteration of the normal organization as well as gliosis.


What is "pseudolaminar necrosis?"

Uneven destruction of the neocortex with preservation of some of the layers.


How does ischemia eventually lead to neuronal death?

Ischemia leads to the release of exitatory amino acid receptors like glutamate which will overstimulate and NDMA and AMPA receptors. This leads to uncontrolled influx of calcium (which activates a ton of catabolic enzymes), and make reactive oxygen species like synthesis of NO and cause cell death eventually.


What is the general idea of cerebral ischemia or infarction?

Occlusions of specific arteries supplying the brain, and recovery depends on how quickly that occlusion is removed.


What is TIA?

Transient Ischemia Attack, referring to reversal of neuronogical function soon after an occlusion presented in the vasculature of the brain. Basically a brief attack that is reversible.


Can TIA's cause convulsive ischemic neurologic disturbances? How long do they last?

They do not cause convulsions, they generally last from 2-15 mins but can theoritically last for hours up to 24 hrs. Can be a few attacks or several hundred.


What is a stroke caused by a full occlusion of a vessel called? Main reason why this is caused?

Cerebral thrombosis, this is due mainly to atherosclerosis, which is frequently associated with HTN and diabetes.


What is the site of origin that is most common for a cerebral thrombosis?

Carotid bifurcation, origin of the middle cerebral artery and either ends of the basilar arteries.


How do thrombotic infarts look? How would you treat it?

Pale infarcts, no bleeding involved, looks bland or anemic and is associated with a thrombus. Tx with anti-coag.


How would the brain present grossly after a thrombotic infarct 2 days after? 2-10 days after? 10 days to 3 weeks?

2 days after the affected area will be pale, soft and swollen. 2-10 days it will be gelatinous and friable but the edema will resolve. after 10 days the tissue will liquify leaving fluid filled cavity lined by dark gray tissues.


How do thrombotic infarcts present histologically?

After 12 hours red neurons appear, there will be cytotoxic and vasogenic edema where endothelial and glial cells swell, and myelinated fibers begin to disintegrate.


What presents up to 48 hrs after a thrombotic infarct histologically?

Neutrophils come first and towards the end of the second day macrophage numbers increases neutrophils decreases until macrophages take over.


2-3 weeks after thrombotic infarct histologically? What happens at the 1 week mark?

Macrophages are stuffed with broken down myelin. At one week reactive astrocytes appear. Not gliosis yet.


What happens in months after a htrombic infarct?

In walls of cystic cavity astrocyte processes form networks of fibers + capillaries + connective tissue --> Gliosis.


What are embolic infarctions?

Most common cause of cerebral embolism are emboluses from a thrombus from heart, from an MI or a-fib or valvular disease.


Which is the most common site of embolic infarction?

MCA, middle cerebral artery.


Other rare causes of embolisms besides the heart which is the most common?

Fat, tumor cells, fibrocartilage, amniotic fluid or air. Trauma can cause bone marrow emboli in white matter.


Another name for Embolic infarcts?

Hemorrhagic infarcts.


How do hemorrhagic infarcts present?

Red, has multiple petecchial hemorrhages that are associated with embolism.


Why do these hemorrhagic infarctions bleed?

Due to reperfusion to damaged vessels through collatoral blood flow or unclotting the clot.


What are lacunar infarcts highly associated with?



If there is a stroke that occludes the MCA, where are the areas of lesions?

Motor cortex - upper limbs and face.
Sensory cortex - upper limbs and face.
Wernicke's area and Broca's area.


How would an occlusion to the MCA present symptomatically?

Contralateral paralysis and loss of senssation of upper limbs and face. Hemineglect if lesion affects non dominant side of brain.


ACA occlusion will affect what areas? How does it present?

Sensory and motor cortex of the lower limbs. It will therefore present as loss of sensation and paralysis of the contralateral lower limbs.


What happens if there is an infarct in the lateral striate artery?

The area of lesion would be the stratium and internal capsule, and this will result in contralateral weakness or paralysis.


What causes the lateral straite artery to be occluted?

It is a common location of a lacunar infarct, which is secondary to HTN.


What happens if there is occlusion of the AComm?

Common site of berry anneurysms --> it will impinge on cranial nerves. Lead to visual field defects and are common of anneurysms, not strokes.


What happens if there is an occlusion in the PComm?

Also a common site of berry anneurysmss, CN3 palsy will result and the eye is "down and out." Again this isnt due to strokes but aneurysms.


If there is a lesion in the ASA what happens?

Area of lesion will be the lateral CST, medial lemniscus and caudal medulla - hypoglossal nerve. There will be contralateral weakness of lower limbs, decreased contralateral proprioception and ipsilateral tongue dysfunction (tongue will deviate ipsilaterally).