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NEUROLOGY REVIEW > Cerebrovascular Disease > Flashcards

Cerebrovascular Disease Flashcards

1
Q

Critical level of cerebral blood flow for infarction?

A

23 mL/100g/min

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2
Q

Normal level of Cerebral blood flow

A

55 ml/10g/min

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3
Q

Reduction of cerebral blood flow to this level causes infarction, almost regardless of its duration

A

10-12 ml/100g/min

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4
Q

A cerebral blood flow of this range causes marked ATP depletion, increased intracellular K, increase in intracellular Ca, cellular acidosis, invariably leading to histologic signs of necrosis

a. 3-5 mL/100g/min
b. 6-8 mL/100g/min
c. 10-12 mL/100g/min
d. 12-23 mL/100g/min

A

b. 6-8 mL/100g/min

page 811

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5
Q

Type of edema that occurs in cerebral infarction

A

cytotoxic edema

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6
Q

The following are changes that occur in the infarcted tissue at critical levels of cerebral blood flow, except:

a. increase in extracellular K
b. increase in intracellular K
c. increase in intracellular Ca
d. cellular acidosis

A

b. increase in intracellular K

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7
Q

These neurotransmitters play a role in stroke, formed from glycolytic intermediates of the Krebs Cycle and are released by ischemic cells, excite neurons and produce intracellular influx of Na and Ca

A

Glutamate and Aspartate

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8
Q

10% of cases of Fibromuscular dysplasia have been reported to be familial and associated with a variant of this gene

A

PHACTR1

Phosphatase and actin regulator 1 gene

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9
Q

Most frequently involved vessel in fibromuscular dysplasia

A

internal carotid artery

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10
Q

series of transverse constrictions appearing as an irregular string of beads or a smooth tubular narrowing is a radiographic feature of this disease

A

Fibromuscular dysplasia

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11
Q

Familial component has been suspected in Moyamoya disease at it is associated with this chromosome

A

Chromosome 17q

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12
Q

A wide degeneration of cerebral white matter having a vascular causation and observed in the context of hypertension, atherosclerosis of the small blood vessels and multiple strokes

A

Binswanger disease

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13
Q

Mutation associated with CADASIL

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy

A

Chromosome 19 of the NOTCH 3 gene

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14
Q

Pathologic finding in skin biopsy in cases of CADASIL

A

eosinophilic inclusions in the arterioles of a skin biopsy

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15
Q

Mutation in CARASIL

Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy

A

HTAR1 gene

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16
Q

oral contraceptives containing this hormone are at increased risk for stroke

a. estrogen
b. progestin

A

a. estrogen

17
Q

fundoscopic finding in hypertensive hemorrhage, ruptured aneurysm, AV malformation or severe cranial trauma

A

preretinal (subhyaloid) hemorrhages

18
Q

Most sensitive means of demonstrating an aneurysm

A

digital subtraction angiography

19
Q

Gene that has been identified as causative for familial inheritance of cavernous malformations

A

KRIT1

20
Q

Safe target of BP in management of hypertensive encephalopathy is a pressure of

A. 160/100 mmhg or a 20% reduction in mean pressure
B. 150/100 mmhg or a 20% reduction in mean pressure
C. 160/100 mmhg or a 10% reduction in mean pressure
D. 150/100 mmhg or a 10% reduction in mean pressure

A

B.

Page 883

21
Q

Transverse sinuses are usually asymmetrical. slightly half of individuals have a dominant _______ vein.

A. Right
B. Left

A

A. Right

22
Q

Syndrome which is an arteriopathy producing deep blue-red skin lesions of livedo reticularis and livedo racemosa in association with multiple ischemic strokes. Many would have high titers of antiphospholipid antibodies`

A

Sneddon Syndrome

23
Q

Recommended treatment for TTP Thrombotic Thrombocytopenic Purpura

A

Plasma Exchange

24
Q

Gene associated with cerebral amyloid angiopathy

A

Homozygous APOE e4/1e4 genotype

25
Q

autoantibodies to this protein is the most specific for detecting Antiphospholipid antibody syndrome

a. lupus anticoagulant
b. anticardiolipin
c. B2-glycoprotein 1
d. ANA

A

c. B2 glycoprotein 1

26
Q

Risk of bleeding from a known AV malformation

% per year

A

3% per year

27
Q

Most common cerebral vascular malformation

a. AV malformation
b. Dural AV Fistula
c. Cavernous Malformation
d. Deep Venous malformation

A

D. Deep venous malformation

estimated to occur at 3%

28
Q

Duration of antibiotic or antifungal treatment for mycotic aneurysm

A

6 weeks

29
Q

This is the volume of blood flowing in a specific amount of brain (100g) in a specified time (sec)

A

cerebral blood flow

30
Q

this is the volume of circulating intravascular blood (ml) in a specified amount of brain

A

cerebral blood volume

31
Q

The mean time for an intravascular particle to transit a specified amount of brain

A

Vascular Mean transit time

32
Q

Which of the vascular modification is being described:

Acellular necrotic core (cellular debris)
Necrotic core is covered by a thick fibrous cap: SMCs in proteoglycan-collagen matrix

a. intimal thickening
b. fatty streak
c. fibroatheromas
d. vulnerable plaque

A

c. fibroatheroma

33
Q

Which of the vascular modification is being described:

Abundant macrophage foam cells mixed with SMCs and proteoglycan-rich intima

a. intimal thickening
b. fatty streak
c. fibroatheromas
d. vulnerable plaque

A

b. fatty streak

34
Q

Which of the vascular modification is being described:

Layers of SMCs and extracellular matrix
more frequent in coronary artery, carotid artery, abdominal aorta, descending aorta, and iliac artery

a. intimal thickening
b. fatty streak
c. fibroatheromas
d. vulnerable plaque

A

a. intimal thickening

35
Q

Which of the vascular modification is being described:

Thin cap fibroatheroma
Type I collagen, very few/absent SMCs
Fibrous cap thickness is <65um

a. intimal thickening
b. fatty streak
c. fibroatheromas
d. vulnerable plaque

A

d. vulnerable plaque

36
Q

Key pathological finding in lacunar stroke

A

lipohyalinosis

37
Q

‘Clumsy hand dysarthria’ stroke is a lacunar syndrome localized in:

a. ipsilateral paramedian pons
b. contralateral paramedian pons
c. ipsilateral posterior limb of the internal capsule
d. contralateral genu of the internal capsule
e. none of the above

A

b. contralateral paramedian pons

38
Q

Stroke in these region(s) may present as hemiparesis with ataxia on the same side as the weakness:

a. lacunar infarct of the midbrain
b. lacunar infarct of the pons
c. lacunar infarct of the internal capsule
d. lacunar infarct of the parietal white matter
e. all of the above

A

e. all of the above

39
Q

optimal timing for restarting anticoagulant treatment in patients with AF who have survived an ICH is`

A

7-8 weeks after hemorrhage

NEUROLOGY REVIEW (24 decks)

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