Lectures 62-63: Cerebrovascular Disease Flashcards

1
Q

Thromboembolus is often…why? Particularly what territory?

A

Hemorrhagic –> when the clot recedes, blood flows into damaged tissue; carotid

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2
Q

Thrombosis is different from thromboembolus how? Particularly in what territory?

A

Local (clot forms over local plaque); posterior circulation

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3
Q

Acute infarct: histological appearance; what it leads to that is dangerous; timeline for peak edema

A

Pallor, edema, early PMNs; can lead to swelling and herniation; 24 - 48 hours

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4
Q

Subacute infarct: cellular and tissue response; timeline

A

Macrophage infiltration, vascular proliferation; demarcation, organization, contraction; organization happens over days - months

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5
Q

Chronic/remote infarct forms what and this leads to what (proper name)

A

Cystic cavity and neural (Wallerian) degeneration

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6
Q

1 cm cubic infarct takes…to reabsorb

A

3 months to reabsorb

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7
Q

Axonal swelling manifests largely in what phase?

A

Subacute

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8
Q

What is a paradoxical finding sometime present in stroke?

A

Enlargement of LV due to blocked foramen, contributes to mass effect

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9
Q

Duret hemorrhage and outcome

A

Process of hemorrhage leading to small infarcts or bleeds in midline brainstem region due to downward displacement of brainstem; outcome generally fatal

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10
Q

Important sign of uncal herniation

A

Blown pupil

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11
Q

Subpial sparing is present in what kind of stroke? Differentiates what?

A

Small amount of spared tissue near pia present in a cerebral stroke; differentiates stroke from trauma

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12
Q

Most common causes of cerebral and meningeal hemorrhage (4)

A

Trauma, vascular malformation (berry aneurysm, malformation), blood dyscrasia, arterial changes (hypertension and amyloid angiopathy)

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13
Q

Blood dyscrasia is often seen in what setting and include what thing?

A

Hospital –> coagulation problem

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14
Q

Arterial changes are chronic/acute

A

Chronic

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15
Q

Vascular lipohyalinosis (def)

A

Weakened arterial wall due to long-term hypertension

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16
Q

Charcot Bouchard aneurysm (def). Most common location?

A

Small aneurysms that arise due to vascular lipohyalinosis; lenticulostriate vessels of basal ganglia

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17
Q

~70% of HT-related hemorrhages are in…

A

Deep gray matter of cerebral hemispheres

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18
Q

Congophilic angiopathy (def)

A

Abnormal deposition of amyloid in cortical/leptomeningeal arterioles

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19
Q

Where do we find congophilic angiopathy hemorrhages? What age?

A

“Lobar” hemorrhages = peripheral cerebral regions; older adults

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20
Q

Two complications of cerebral hemorrhage

A
  1. Rupture into ventricular system; 2. Vasopasm leading to secondary infarction
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21
Q

If neither complication happens, what is the resolution of a cerebral hemorrhage? This is unlike…

A

Slit-like (small) cavity; unlike an infarct, which leads to cystic cavities

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22
Q

Classifications of global brain hypoxia

A

Stagnant/hypoperfusion (reduced or no flow) or hypoxic/anoxic (reduced or no O2, such as due to CO poisoning)

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23
Q

Global brain hypoxia cause also be… (3)

A

Anemic (due to a bleed elsewhere), histotoxic (nitrogen “bends”), hypoglycemic

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24
Q

The most important thing to remember in regards to global event?

A

Selective vulnerability of cells

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25
Q

What cell is damaged most rapidly? Where in particular (3)?

A

Pyramidal cells; borderzone arterial territories, deep cortical layers (III, V, VI), hippocampus

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26
Q

Describe cellular selective vulnerability

A

Neurons > oligodendroglia > astrocytes

27
Q

Brain death begins with…which does what? Then what? What happens to the tissue? Can you recover from brain death?

A

Diffuse cerebral edema; increased intracranial pressure; blood flow blocked; it begins autolysis (liquefaction); NO

28
Q

What is the difference between persistent vegetative state and brain death?

A

Brain death has not happened because it never lost perfusion; vegetative state = spontaneous eye opening, sleep-wake cycles, maintain breathing

29
Q

Three most common causes of stroke

A

Cardioembolic (embolism from heart), atherosclerotic, lacunar (small vessel stroke)

30
Q

Risk factors (5)

A

Hypertension, heart disease, carotid bruit, diabetes, smoking

31
Q

Best predictor of stroke

A

Previous stroke

32
Q

Leading stroke risk factor for women and modifiable women-specific stroke risk factors

A

Migraine with aura; oral contraceptives

33
Q

Ischemic stroke definition and typical cause

A

Low blood flow to focal part of the brain; thromboembolism

34
Q

How much stroke is ischemic (%)

A

85%

35
Q

Core of stroke…

A

Does not recover

36
Q

What region of the stroke may be salvageable?

A

Penumbra around core; this is why we must treat quickly

37
Q

What is the border of the stroke called?

A

Benign oligemia

38
Q

ACA stroke (arm and leg)

A

Leg > arm

39
Q

MCA gives rise to which important distribution? Where?

A

Lenticulostriate (internal capsule and basal ganglia)

40
Q

MCA stroke (arm and leg)

A

Arm > leg

41
Q

Left (dominant) cerebral hemisphere symptoms (4)

A

Aphasia, L graze preference (look at stroke), R visual field deficit, R hemiparesis/sensory loss

42
Q

“Anterior circulation” stroke includes which two artery involvement?

A

ACA/MCA

43
Q

Right (nondominant) cerebral hemisphere (4)

A

R gaze preference (look at stroke), L visual field deficit, L hemiparesis/sensory loss, NEGLECT (L hemi-inattention and anosagnosia)

44
Q

What is an internal carotid artery occlusion typically preceded by and course of this? What other symptoms (aka, arteries)?

A

Amaurosis fugax: gray shade dropping over the eye; demonstrates that presence of carotid artery occlusion –> reduced retinal circulation –> blindness (retinal hypoxia); anterior = MCA and ACA symptoms

45
Q

PCA syndrome (contralateral, dominant, and bilateral)

A

Contralateral = homonymous hemianopsia w/ macular sparing; Dominant = alexia w/out agraphia; Bilateral = Anton’s syndrome

46
Q

Brainstem stroke can cause what kinds of paresis/sensory loss

A

Hemi- or quadri-

47
Q

Emboli are more frequent in posterior or anterior vertebral circulation?

A

Anterior

48
Q

Acute cerebellar infarction: presents as…but one important consideration

A

Often doesn’t look so bad on presentation; can develop life-threatening edema due to ventricular system/brainstem obstruction

49
Q

Stroke where causes locked-in syndrome. What vessel?

A

Pons; basilar artery

50
Q

Is a persistent vegetative state a coma?

A

Yes

51
Q

Lacunar infarcts and locations (4)

A

Pure motor (posterior IC), pure sensory (thalamus), dysarthria/clumsy hand syndrome (pons), ataxic hemiparesis (plantar cerebellar/corticospinal)

52
Q

Transient ischemic attack (TIA)

A

Reversible focal dysfunction defined as less than 24 hours; should initiate stroke therapy (linked to stroke in coming days)

53
Q

Subarachnoid hemorrhage; symptoms (3)

A

Bleeding around brain, typically caused by aneurysm; “worst headache of the life,” N/V, neck stiffness

54
Q

Types of aneurysms (3)

A

Berry, mycotic (due to infection), Charcot-Bouchard (micro-aneurysms usually in lenticulostriates associated with hypertension)

55
Q

Berry aneurysms are most commonly found…%

A

At juncture between anterior communicating and ACA (40%)

56
Q

Intracerebral hemorrhage most commonly caused by…

A

Chronic hypertension

57
Q

Carotid dissection (def)

A

Two layers of carotid wall separate causing luminal narrowing + formation of blood clot

58
Q

How to evaluate for tPA…can’t use in what situation? What about platelets?

A

Hemorrhage; if platelets are less than 100,000, no tPA

59
Q

General principles of stroke treatment…

A
  1. 85% are ischemic, 2. Most caused by clot, 3. Ischemic penumbra = time is brain
60
Q

tPA timeline

A

> 3 hours = IV tPA; 3-6 hours = IA tPA; >6 hours = endovascular intervention

61
Q

Which, IV or IA, is better? IA requires what?

A

IV; IA requires angiogram

62
Q

Aspirin is used to prevent…

A

Recurrent ischemic strokes

63
Q

What’s a good pneumonic for remembering what limb ACA and MCA have a preference for?

A

Alma (like alma mater) = anterior leg, middle arm