vascular disorders Flashcards

1
Q

What vessels are involves in anterior circulation of cerebrum?

A

internal carotid A
anterior cerebral A
middle cerebral A

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2
Q

What vessel are involved in posterior circulation?

A

vertebral A
basilar A
posterior cerebral A

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3
Q

Where and when do watershed infarcts occur?

A

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

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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,

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5
Q

What are the most common sources of thromboembolism?

A

cardiac:
a. fib
MI
bacterial endocarditis/septic emboli

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6
Q

What are some noncardiac sources of thromboemboli?

A

major artery atheromatous plaques
fat emboli
air emboli

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7
Q

Why are cerebral infarcts commonly hemorrhagic?

A
  1. fragmentation/detachment of embolic material from initial site of impaction and,
  2. repurfusion
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8
Q

What are some results/consequences of septic emboli?

3Ms

A

meningitis and microabscesses

mycotic aneuysms- infected vessel walls

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9
Q

What are transient ischemic attacks? What causes them?

A

mini strokes caused by plt emboli from a atherosclerotic plaque.

ischemia without infarction

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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.

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11
Q

What are the characteristic clinical features of cerebral infarction?

A

sudden onset- vascular suggestion

deficits reflect affected vascular territory

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12
Q

Outline the steps of the macroscopic pathology of cerebral infarction:

A

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

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13
Q

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

A

coagulation necrosis leading to red-dead neurons

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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@.

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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@

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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?

A

HYP and DM

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
Q

Describe the pathogenesis of hyp hemorrhages? Where do they commonly occur?

A

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
Q

If CNS element’s involvement, causes hyp hemorrhages to be more fatal?

A

lateral ventricle

27
Q

What is commonly seen in the deep penetrating arteries of HYP hemorrhages?

A

Charcot- Bouchard aneurysms

28
Q

What space do hemorrhages from saccular aneurysms occur in CNS?

A

subarachnoid

29
Q

What is the classical clinical picture of a saccular berry aneurysm?

A

middle aged, no preexisting conditions
worst headache of life
stiff neck- meningismus

30
Q

Where do saccular aneurysms occur? Most common locations?

A

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
Q

What causes the formation of saccular berry aneurysm?

A
  1. developmental defect of media/elastica, and

2. repeated/prolonged hemodynamic stress

32
Q

Commonly presenting with hemorrhages and seizures in 20’s/30’s are what?

A

arteriovenous malformations resulting from abl maturation of vessels during development.

33
Q

What does this malformation result in grossly?

A

tangle of abl arteries, veins and communicating shunts, leaving the pt predisposed to bleeding.

34
Q

Histologically, how does arteriovenous malformation present?

A

large arteries and thick walled veins with intervening brain tissue

35
Q

What is the radiographical appearance of cavernous malformation?

A

dark rim on MRI

36
Q

What is the histological appearance of a cavernous sinus?

A

dilated venous/capillary channels,
and a rim of hemosiderin,
minimal intervening brain tissue

37
Q

Cerebral amyloid angiopathy is described as?

A

An elderly- alzheimer associated, often familial- cause of lobar hemorrhage