Neuropath IV Flashcards

1
Q

What is Charcot-Bouchard micro-aneurysm?

A

segmental dilation of small vessels due to hypertension

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2
Q

What are the frequent sites of hypertensive intraparenchymal hemorrhage? Source?

A

basal ganglia, thalamus, cerebellum, and basis pontis. Many begin in the external capsule or putamen, probably due to Charcot-Bouchard microaneuyrsms of the lenticulostriate arteries.

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3
Q

What is a saccular aneurysms? Predispostion?

A

malforations of vessels at the branch points. some may be familial or associated with genetic disease (Ehlers Danlos, neurofibromatosis typi I, Marfan, etc.), HTN, arteriovenous malformations.

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4
Q

What are the major locations of saccular aneurysm?

A

MOST in the ANTERIOR circulation (all 3 about equally likely):
1. anterior cerebral and anterior communicating junction
2. bifurcatio of the internal carotid artery/juction with the PCom
3. bifurcation/trifurcation of the middle cerebral artery
(tip of the basilar artery in posterior circ)

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5
Q

Berry/saccular aneurysms are the most common cause of _____.

A

spontenous subarachnoid hemorrhage, especially at the base of the brain.

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6
Q

What happens in acute rupture of saccular aneurysms? Clinical finding?

A

subarachnoid hemorrhage, rapid rise in intracranial pressure, severe headache

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7
Q

What happens in minor/repetitive saccular aneurysms?

A

may be bound to brain surface. more foreceful bleeds can go into the brain parenchyma

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8
Q

What are complications of aneurysm rupture? When do they occur?

A

death

vasospasm- 4-10 days after rupture. Leads to infarction. hydrocephalus from impaired CSF flow.

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9
Q

Besides berry aneurysms, what are other forms of aneurysms in the brain?

A

fusiform (aka atherosclerotic)

infectious (mycotic, septic)

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10
Q

What should I know about fusiform aneurysms? location, causes/disease process, clinical significance

A

Usually in vertebrobasilar arteries
due to advanced atherosclerosis and the changes of the arteries that are seen in the context of atherosclerosis, such as becoming elongated, tortuous (emphasized), and dilated.
usually asymptomatic, rarely rupture, may compress cranial nerves or be source of thromboemboli.

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11
Q

What should I know about infectious aneurysms?

A

secondary to bacerial emboli. rare. usually multiple

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12
Q

What are the 4 kinds of vascular malformations?

A

arteriovenous malformation, cavernous malformation, venous angioma, and capillary telangiectasia

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13
Q

What are the clinical manifestations of vascular malformations?

A

spontaneous subarachnoid or intraparenchymal hemorrhage, seizure, or focal neurological defects.

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14
Q

What are the most common vascular anomalies?

A

arteriovenous malformations. especially seen supratentorially, esp. in the lateral cerebral hemisphere. artery and veins connected w/o capillary beds in the middle

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15
Q

Describe arteriovenous malformations (ie. describe what the vessels are like).

A

tangled mass of dilated, thin walled arteries. thickened arterialized veins with intervening gliotic brain parenchyma. may have local ischemia or local hemorrhages. dynamic lesions

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16
Q

What is cavernous malformation? gross lesions, microscopic lesions, who gets it?

A

supratentorial lesions. circumscribed anomalies that look like dark red, spongy lesions on gross specimens.
Microscopically, back to back venous structures packed together without intervening neural parenchyma. often multiple, familial, and also located in other parts of the body
popcorn appearence

17
Q

What should I know about venous angiomas and capillary telangiectasias?

A

both are usually asymptomatic. venous angiomas are just really big veins, usually.
capillary telengiactesias resemble petechiae

18
Q

What is cerebral amyloid angiopathy? Population? associated symptoms?

A

amyloid deposition in the corticomeningeal arteries, arterioles and other vessels. seen in many elderly ppl and in Alzheimers. increased risk of cerebral hemorrhages, usually multiple and LOBAR in distribution. (bleeding often in the cerebral white matter)

19
Q

What is CADASIL?

A

cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. headaches that eventually progress to dementia. Notch mutation