Cerebrovascular Disease Flashcards
Critical level of cerebral blood flow for infarction?
23 mL/100g/min
Normal level of Cerebral blood flow
55 ml/10g/min
Reduction of cerebral blood flow to this level causes infarction, almost regardless of its duration
10-12 ml/100g/min
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
b. 6-8 mL/100g/min
page 811
Type of edema that occurs in cerebral infarction
cytotoxic edema
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
b. increase in intracellular K
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
Glutamate and Aspartate
10% of cases of Fibromuscular dysplasia have been reported to be familial and associated with a variant of this gene
PHACTR1
Phosphatase and actin regulator 1 gene
Most frequently involved vessel in fibromuscular dysplasia
internal carotid artery
series of transverse constrictions appearing as an irregular string of beads or a smooth tubular narrowing is a radiographic feature of this disease
Fibromuscular dysplasia
Familial component has been suspected in Moyamoya disease at it is associated with this chromosome
Chromosome 17q
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
Binswanger disease
Mutation associated with CADASIL
Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy
Chromosome 19 of the NOTCH 3 gene
Pathologic finding in skin biopsy in cases of CADASIL
eosinophilic inclusions in the arterioles of a skin biopsy
Mutation in CARASIL
Cerebral autosomal recessive arteriopathy with subcortical infarcts and leukoencephalopathy
HTAR1 gene
oral contraceptives containing this hormone are at increased risk for stroke
a. estrogen
b. progestin
a. estrogen
fundoscopic finding in hypertensive hemorrhage, ruptured aneurysm, AV malformation or severe cranial trauma
preretinal (subhyaloid) hemorrhages
Most sensitive means of demonstrating an aneurysm
digital subtraction angiography
Gene that has been identified as causative for familial inheritance of cavernous malformations
KRIT1
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
B.
Page 883
Transverse sinuses are usually asymmetrical. slightly half of individuals have a dominant _______ vein.
A. Right
B. Left
A. Right
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`
Sneddon Syndrome
Recommended treatment for TTP Thrombotic Thrombocytopenic Purpura
Plasma Exchange
Gene associated with cerebral amyloid angiopathy
Homozygous APOE e4/1e4 genotype
autoantibodies to this protein is the most specific for detecting Antiphospholipid antibody syndrome
a. lupus anticoagulant
b. anticardiolipin
c. B2-glycoprotein 1
d. ANA
c. B2 glycoprotein 1
Risk of bleeding from a known AV malformation
% per year
3% per year
Most common cerebral vascular malformation
a. AV malformation
b. Dural AV Fistula
c. Cavernous Malformation
d. Deep Venous malformation
D. Deep venous malformation
estimated to occur at 3%
Duration of antibiotic or antifungal treatment for mycotic aneurysm
6 weeks
This is the volume of blood flowing in a specific amount of brain (100g) in a specified time (sec)
cerebral blood flow
this is the volume of circulating intravascular blood (ml) in a specified amount of brain
cerebral blood volume
The mean time for an intravascular particle to transit a specified amount of brain
Vascular Mean transit time
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
c. fibroatheroma
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
b. fatty streak
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. intimal thickening
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
d. vulnerable plaque
Key pathological finding in lacunar stroke
lipohyalinosis
‘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
b. contralateral paramedian pons
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
e. all of the above
optimal timing for restarting anticoagulant treatment in patients with AF who have survived an ICH is`
7-8 weeks after hemorrhage
