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NEURO 411 > Neurodegenerative Cerebrovascular Disease > Flashcards

Neurodegenerative Cerebrovascular Disease Flashcards

1
Q

What is lacunar stroke? What is the size of this stroke? Where does it primarily occur?

A
  • small vessel disease of the penetrating artery
  • <15mm
  • subcortical or brainstem
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2
Q

What is lacunar stroke pathology?

A
  • arteriolosclerosis, lipohyalinosis, fibrinoid necrosis
  • perivascular inflammatory cells
  • microatheroma
  • endothelial dysfunction
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3
Q

What are some small vessel diseases other than lacunar stroke?

A
  • white matter Hyperintensities
  • dilated perivascular space
  • microhemorrhage
  • microinfarcts
  • cerebral atrophy
  • microvascular disease of other organs (renal, cardiac, retinal disease)
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4
Q

What are the clinical manifestations of lacunar stroke and CSVD? What percentage of ischemic strokes does it account for? What percentage of dementia does it account for?

A
  • stroke
  • cognitive decline
  • gait impairment
  • 20% of ischemic strokes
  • 45% of dementia
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5
Q

What are some imaging features of CSVD? (also see diagram on slide 30)

A
  • lacunar stroke
  • white matter hyperintensities
  • microhemorrhage
  • dilated perivascular space
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6
Q

What can you visualize for CSVD using high res MRI?

A
  • microinfarcts
  • DTI: altered white matter integrity,
    altered myelination, free water
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7
Q

What is the proposed mechanism of CSVD?

A
  • ischemia –> occlusion –> thrombosis, vasospasm, impaired autoregulation, hypoperfusion
  • endothelial failure –> increased permeability –> Perivascular infiltration, vessel injury, inflammation, impaired autoregulation, luminal narrowing / occlusion
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8
Q

How is hypertension related to CSVD?

A

ENDOTHELIAL DYSFUNCTION IN BRAIN SMALL VESSELS
- Enhanced permeability / plasma extravasation
- Increased leukocyte adhesion
- Fibrin deposition (lipohyalinosis, fibrinoid necrosis)
- Autoregulation impaired, reduced vasodilatory capacity
- Arteriolar thrombosis

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9
Q

How is inflammation related to CSVD?

A
  • Inflammation affects endothelium and Blood Brain Barrier
  • Inflammatory makers are increased in lacunar stroke and associated with WMH progression
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10
Q

salt promotes ______, ___________, ______________.

A

oxidative stress, inflammation, small vessel dz

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11
Q

___________________ precede(s) hypertension in SHRSP.

A

small vessel changes

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12
Q

What are treatments of CSVD? Are there any treatments specific to CSVD?

A
  • BP control
  • single antiplatelet
  • vascular disk factor management
  • no specific treatment
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13
Q

slide 18???

A

What is happening lol

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14
Q

What are the causes of endothelial dysfunction in patieints with CSVD?

A
  • hypertension
  • diabetes
  • inflammation
  • genetics
  • impaired endothelial support (Astrocytes, Pericytes, Neurons, Oligodendrocytes, ECM)
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15
Q

TRUE or FALSE: WMH is heritable

A

TRUE

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16
Q

know genes from slide 20????

A
17
Q

TRUE or FALSE: BP control alone can improve endothelial function

A

FALSE: Blood pressure predicts progression of WMH. However antihypertension treatment has limited effect on slowing WMH
progression

18
Q

What is cerebral amyloid angiopathy? What risk is it associated with?

A
  • amyloid deposition in cerebral vasculature
  • increased risk of cognitive impairment and ICH
19
Q

What are the MRI features of cerebral amyloid angiopathy?

A
  • cortical superficial siderosis
  • lobar intracerebral hematoma
  • convexity subarachnoid hemorrhage
  • white matter disconnection
  • atrophy
  • lobar microbleeds
20
Q

chart on slide 24???

A
21
Q

What is the modified boston criteria for definite CAA?

A

Full postmortem exam demonstrating:
- lobar, cortical or cortical-subcortical hemorrhage
- severe CAA with vasculopathy
- absence of other diagnostic lesion

22
Q

What isthe modified boston criteria for probably CAA with supporting pathology?

A

Clinical data and pathological tissue demonstrating:
- lobar, cortical, or cortical-subcortical hemorrhage
- some degree of CAA
- absence of other diagnostic lesion

23
Q

What is the modified Boston criteria for probable CAA?

A

Clinical data and MRI or CT demonstrating:
- MULTIPLE hemorrhages restricted to lobar, cortical, or cortical-subcortical hemorrhage and cSS
- age > 55
- absence of other cause of hemorrhage

24
Q

What is the modified Boston criteria for possible CAA?

A

Clinical data and MRI or CT demonstrating:
- SINGLE lobar, cortical, or cortical-subcortical ICH, CMB, or cSS
- age > 55
- absence of other cause of hemorrhage

25
Q

What are the types of sporadic CAA?

A

type 1 and type 2

26
Q

What are the familial types (genes) of CAA ? - probably don’t have to know lol

A
  • E693Q (Dutch), E693K (Italian), and L705V (Piedmont)
  • E693G (Arctic) and D694N (Iowa)
  • E693Q (HCHWA-D)
27
Q

continue slide 27

A

NEURO 411 (12 decks)

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