vascular disorders Flashcards

(37 cards)

1
Q

What vessels are involves in anterior circulation of cerebrum?

A

internal carotid A
anterior cerebral A
middle cerebral A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What vessel are involved in posterior circulation?

A

vertebral A
basilar A
posterior cerebral A

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where and when do watershed infarcts occur?

A

Bw distributions of anterior and middle cerebral arteries when diffuse hypotension occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is a common cause of cerebrovascular thrombosis? What are major sites of involvement?

A

arterial atherothrombosis, often involving:

internal/external carotid bifurcation, m.cerebral A,
vertebrobasilar A,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the most common sources of thromboembolism?

A

cardiac:
a. fib
MI
bacterial endocarditis/septic emboli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are some noncardiac sources of thromboemboli?

A

major artery atheromatous plaques
fat emboli
air emboli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Why are cerebral infarcts commonly hemorrhagic?

A
  1. fragmentation/detachment of embolic material from initial site of impaction and,
  2. repurfusion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are some results/consequences of septic emboli?

3Ms

A

meningitis and microabscesses

mycotic aneuysms- infected vessel walls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What are transient ischemic attacks? What causes them?

A

mini strokes caused by plt emboli from a atherosclerotic plaque.

ischemia without infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the clinical definition of TIAs?

A

episodes of neurological dysfunction that last a few minutes to an hour, and completely return by 24 hours.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the characteristic clinical features of cerebral infarction?

A

sudden onset- vascular suggestion

deficits reflect affected vascular territory

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Outline the steps of the macroscopic pathology of cerebral infarction:

A

1- softening and edema-> herniation
2- necrosis
3- cyst-like cavitaion

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the important microscopic feature of the first 12-48 hours following CI?

A

coagulation necrosis leading to red-dead neurons

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the important microscopic features of the 3-7 days following CI?

A

m@ and PMNs begin liquefaction necrosis-

from circulation, phagocytize necrotic debris and become liquid laden m@.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What are the important microscopic features of the 7-14 days following CI?

A

vascular proliferation and liquefaction necrosis,

reactive astrocytes and more m@

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

When does organizing cavitation occur? What are they surrounded by?

A

weeks to months

reactive astrocytes

17
Q

What vessels are occluded causing lacunar infarcts?

A

deep paramedian penetrating arteries

18
Q

Where do lacunar infarcts occur? What histological changes do they cause?

A

lipohyalinosis ateriolosclerosis

19
Q

What diseases are lacunar infarcts associated with?

20
Q

What are the variants of venous infarcts?

A

lacunar

venous

21
Q

What typically results from a venous infarction?

A

Hemorrhagic infarction

22
Q

What conditions/states often precipitate superior sagittal sinus thrombosis (SSST)? What can SSST cause?

A

infection
dehydration

bilateral parasagittal hemorrhagic cerebral infarcts

23
Q

What is the pathogenesis of venous infarcts?

A

rapid thrombotic occlusion of deep cerebral veins/venous sinuses causing diminished flow/venous congestion–> ischemia and hemorrhagic infarction

24
Q

What are the clinical aspects of HYP hemorrhages?

A

sudden headache, obtundation

deficits reflective of location

25
Describe the pathogenesis of hyp hemorrhages? Where do they commonly occur?
rupture of Charcot-Bouchard aneurysms that cause displacement of CNS elements, occurs in deep cerebral gray and WM, also occurs deep WM, thalamus, pons and cerebellum
26
If CNS element's involvement, causes hyp hemorrhages to be more fatal?
lateral ventricle
27
What is commonly seen in the deep penetrating arteries of HYP hemorrhages?
Charcot- Bouchard aneurysms
28
What space do hemorrhages from saccular aneurysms occur in CNS?
subarachnoid
29
What is the classical clinical picture of a saccular berry aneurysm?
middle aged, no preexisting conditions worst headache of life stiff neck- meningismus
30
Where do saccular aneurysms occur? Most common locations?
bifurcations of large vessels, especially proximal branches of circle of Willis 1. jnx of: internal carotid- posterior communicating- middle cerebral A 2. jnx: ant. cerebral- ant. communicating A. 3. first branch of m. cerebral A.
31
What causes the formation of saccular berry aneurysm?
1. developmental defect of media/elastica, and | 2. repeated/prolonged hemodynamic stress
32
Commonly presenting with hemorrhages and seizures in 20's/30's are what?
arteriovenous malformations resulting from abl maturation of vessels during development.
33
What does this malformation result in grossly?
tangle of abl arteries, veins and communicating shunts, leaving the pt predisposed to bleeding.
34
Histologically, how does arteriovenous malformation present?
large arteries and thick walled veins with intervening brain tissue
35
What is the radiographical appearance of cavernous malformation?
dark rim on MRI
36
What is the histological appearance of a cavernous sinus?
dilated venous/capillary channels, and a rim of hemosiderin, minimal intervening brain tissue
37
Cerebral amyloid angiopathy is described as?
An elderly- alzheimer associated, often familial- cause of lobar hemorrhage