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Neuro > Vascular disorders > Flashcards

Vascular disorders Flashcards

1
Q

systemic hyperperfusion is caused by

A

global cerebral ischemia

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2
Q

Ischemia at what area causes greatest risk of systemic hypoperfusion

A

Watershed zone between ACA and MCA

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3
Q

signs of systemic hypoperfusion

A

Low BP

pallor

sweating

man in a barrel syndrome

anterograde amnesia

intention tremor

nystagmus

ataxia

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4
Q

morphology of global cerebral ischemia at

12-24 hours

A

Red neurons:

eosinophilic cytoplasm

pyknotic nuclei

loss of Nissl Bodies

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5
Q

morphology of global cerebral ischemia at

1-3 days

A

Neutrophilic Infiltration

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6
Q

morphology of global cerebral ischemia at

3-7 days

A

microglia infiltration and phagocytosis

phagocytes have foamy lipid cytoplasm

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7
Q

morphology of global cerebral ischemia at

1-2 weeks

A

Reactive gliosis by astrocytes

Vascular proliferation around necrotic areas

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8
Q

morphology of global cerebral ischemia at

>2 weeks

A

Glial scaring by astrocytes

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9
Q

Macroscopic morphology of global cerebral ischemia at

1 week to 1 month

A

Liquifactive necroisis

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10
Q

Macroscopic morphology of global cerebral ischemia at

>1 month

A

Cystic cavity surrounded by a wall of dense glial fibers

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11
Q

What causes a stroke

A

focal cerebral ischemia

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12
Q

Types of ischemic stroke

A

Embolic

Thrombotic

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13
Q

Associations of an Embolic Ischemic stroke

A

Afib of the left atrium

Myocardial aneurism

Bacterial endocarditis

Atheroemboli

Cardiac shunts

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14
Q

Cause of thrombotic ischemic stroke

A

atherosclerosis

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15
Q

Morphology of thrombotic ischemic stroke

A

hyaline arteriolosclerosis

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16
Q

Associations of thrombotic ischemic stroke

A

HTN

DM

Lacunar infarcts

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17
Q

Presentation of hypertensive hemorrhages

A

Lacunar infarcts

slit hemorrhages

hypertensive encephalopathy

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18
Q

cause of hypertensive hemorrhage

A

malignant HTN

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19
Q

Acute Morphology of hypertensive hemorrhage

A

central core of clotted blood surrounded by a rim of brain tissue showing axonic neuronal and glial changes, as well as edema

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20
Q

Chronic morphology of hypertensive hemorrhage

A
  • cavitary destruction with a rim of brownish discoloration
  • After edema resolves, hemosiderin and lipid-laden macrophages appear eith proliferation of reactive astrocytes
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21
Q

Location of a pure motor lacunar infarct

A

posterior limb of internal capsule

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22
Q

location of a pure sensory lacunar infarct

A

VPL of the Thalamus

23
Q

location of a Sensorimotor lacunar infarct

A

thalamus

internal capsule

caudate

putamen

pons

24
Q

location of am ataxic hemiparesis lacunar infarct

A

base of the pons

internal capsule

25
Q

location of a dysarthria-clumsy hand syndrome lacunar infarct

A

pons

internal capsule

26
Q

slit hemorrhage morphology

A

slit-like cavity surrounded by a brown discoloration

focal destruction

pigment laden macrophages

gliosis

27
Q

What causes hypertensive encephalopathy

A

malignant HTN

28
Q

What does hypertensive encephalopathy cause

A

cerebellar dysfunction

Progressive HA

N/V

Confusion

Convulsions

Coma

29
Q

Morphology of hypertensive encephalopathy

A

edematous brain, with or without tonsillar herniation

petechiae and fibrinoid necrosis of arterioles in the grey and white matter

30
Q

Sequelae of hypertensive encephalopathy

A
  1. Muli-infarct Dementia
  2. Binswanger Disease
31
Q

causes of Multi-infarct dementia

A

cerebral atherosclerosis

chronic arteriolar sclerosis

vessel thrombi/ emboli from the carotid to the heart

32
Q

Morphology of Binswanger disease

A

large areas of white matter with myelin and axon loss

33
Q

signs of multi-infarct dementia

A

dementia

gait abnormalities

pseudobulbar signs

34
Q

Tyes of hemorrhagic stroke

A

intracerebral stroke (ICH)

Subarachnoid Stroke (SAH)

35
Q

most common spontaneous cause of ICH

A

HTN

36
Q

Most common cause of ICH in kids

A

Ruptured AVM

37
Q

Most common cause of ICH in the elderly

A

Cerebral Amyloid Angiopathy

38
Q

Associations of ICH

A

Coagulation disorders

CNS infection

Neoplasms

Stimulants

Traumatic injury

39
Q
A
40
Q

Etiology of SAH

A

Ruptured berry aneurysm

ruptured AVM

41
Q

Associations of SAH

A

Angiomas

Neoplasms

42
Q

Complications of SAH

A

Rebleeding

Arterial Vasospasm

Hydrocephalus

43
Q

most common cause of ganglionic hemorrhages

A

HTN

44
Q

common locations for ganglionic hemorrhages

A

Subcortical (Deep Brain) Regions

Basal ganglia

Cerebellar Nuclei

Thalamus

Pons

45
Q

sequelae of ganglionic hemorrhage

A
  1. hyaline arteriosclerosis of small penetrating arteries
  2. focal damage or formation of microaneurysms
  3. Charcot Buchard microaneurysms
46
Q

Most common risk factor for lobar hemorrhage

A

cerebral amyloid angiopathy

47
Q

what is cerebral amyloid angiopathy

A

amyloidogenic peptides are deposited in the walls of medium and small meningeal and cortical vessels, which weakens the vessel wall

48
Q

most common locations of lobar hemorrhage

A

occipital lobe

parietal lobe

49
Q

Pathogenesis of a non-ruptured berry aneurysm

A

arterial walls lack internal elastic lamina and media, causing developmental weakness

50
Q

Associations of non-ruptured berry aneurysms

A

Autosomal dominant polycystic kidney disease

Ehlers-Danlos

Marfan Syndrome

Neurofibromatosis Type 1

51
Q

What is an arteriovenous malformation

A

tangled network of vascular channels in the posterior branch of the MCA

52
Q

clinical presentation of AVM

A

young male with CHF in childhood:

seizure

ICH

SAH

53
Q

cavernous malformation morphology

A

popcorn/ mulberry appearance

dilated capillaries with an endothelial lining

thin adventitia with no elastic fibers and smooth muscle

54
Q

Clinical presentation of Cavernous sinus malformation

A

seizure

ICH

SAH

progressive neurologic deficits

inheritance

Neuro (13 decks)

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