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IMC606: Neurology > CVD and Ischemia > Flashcards

CVD and Ischemia Flashcards

IMC 606

1
Q

Blood vessels involved in

Anterior Circulation

A

internal carotid, anterior cerebral, middle cerebral, ophthalmic arteries

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2
Q

Blood vessels involved in

Posterior Circulation

A

vertebral, basilar, posterior cerebral arteries (and their branches)

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3
Q

Define

Focal neurological deficit

A

A deficit that is associated with a specific area of dysfunction/lesion. Examples include: hemi/quadrant anopia, loss of tactile sensation for part of the body, UMN deficits for part of the body, Broca or Wernicke aphasia.

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4
Q

Pathological stages of plaque formation in atherosclerosis

A

Deposition of fat in the intima of vessels – macrophages migrate into area and secrete cytokines to initiate an inflammatory reaction – smooth muscle cells proliferate and connective tissue is deposited – plaque continues to grow in size

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5
Q

What are the pathophysiologic stages of occlusion in small vessels?

A

Lipohyalinosis involves endothelial damage followed by thickening of the vessel wall. This can cause vessel occlusion or formation of microaneurysms.

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6
Q

What are risk factors for lipohyalinosis?

A

Hypertension, diabetes, aging are major risk factors.

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7
Q

What vessels are involved in lipohyalinosis

A

Long, narrow vessels such as lenticulostriates, thalamic perforators, and basilar branches

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8
Q

What is a lacunar stroke?

A

Lacunar strokes are infarcts of small, penetrating blood vessels that result in small lesions deep in the brain.

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9
Q

Where do lacunar strokes occur?

A

They occur along long, narrow penetrating vessels that supply regions such as basal ganglia, internal capsule, diencephalon.

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10
Q

What process contributes to lacunar strokes?

A

Lipohyalinosis contributes to infarcts of these vessels affected by hypertension, diabetes, and age.

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11
Q

What is a TIA?

A

A temporary decrease in blood flow to part of the brain lasting typically about 5 minutes. It may be caused by an embolism that eventually dissolves or a thrombosis.

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12
Q

How can SAH be distinguished from meningitis?

A

SAH does not involve fever and would show RBCs in an LP. CT/MRI may also be helpful to show blood in sulcal spaces vs meningeal inflammation.

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13
Q

Pathological process in

Thombosis

A

Atherosclerosis – fat deposition, fibrosis, occlusion

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14
Q

Pathologic Process in

Small Vessel Occlusion/ Lacunar Infarct

A

Lipohyalinosis – endothelial damage, vessel thickening, occlusion

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15
Q

Pathologic process in

Embolism

A

Dislodged objects circulating in bloodstream

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16
Q

Pathologic Process in

Arterial Dissection

A

Separation of intima and media layers with expanding hematoma

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17
Q

Risk factors in

Thrombosis

A

Hypertension, diabetes, hyperlipidemia, smoking, inflammation

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18
Q

Risk factors in

Small Vessel Occlusion/ Lacunar Infarct

A

Hypertension, diabetes, aging

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19
Q

Risk factors in

Embolism

A

Common sources: Heart and internal carotid artery

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20
Q

Risk factors in

Arterial Dissection

A

Hypertension, trauma, atherosclerosis

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21
Q

Treatment for

Thrombosis

A

tPA, thrombectomy

22
Q

Treatment for

Small Vessel Occlusion/ Lacunar Infarct

A

Control hypertension

23
Q

Treatment for

Embolism

A

Anticoagulants, AF control

24
Q

Treatment for

Arterial Dissection

A

thrombectomy

25
Q

3 criteria for brain death

A

lack of brain function, lack of cranial nerve function, and loss of all brainstem reflexes

26
Q

What is the caloric test?

A

involves infusion of cold/warm water into the external ear canal that stimulates movement of endolymph and thereby elicits the vestibulo-ocular reflex

27
Q

Why is the caloric test used to test brain death?

A

assesses function of a large portion of the brainstem from medulla to midbrain that contains the pathway for this response

28
Q

What reflexes do we test to assess brainstem function?

A

Pupillary light reflex
Corneal reflex
Oculo-cephalic

29
Q

What does the pupillary light reflex test?

A

Midbrain function

30
Q

What does the corneal reflex test?

A

Pons function

31
Q

What does the oculo-cephalic reflex or caloric test assess?

A

Medulla function

32
Q

Location of

Intracerebral Hemorrhage (aneurysm, AVM)

A

Subcortical – basal ganglia, thalamus, brainstem, cerebellum

33
Q

Location of

Subarachnoid Hemorrhage

A

Subarachnoid space

34
Q

Location of

Berry or fusiform aneurysm

A

Circle of Willis, vessel branch locations
Any location

35
Q

Location of

AVM

A

Subcortical or subarachnoid

36
Q

Risk factors for

Intracerebral hemorrhage

A

Hypertension causing microaneurysms, AVM, trauma, tumor

37
Q

Risk factors for

Subarachnoid hemorrhage

A

Trauma
Aneurysm

38
Q

Treatments for

Aneurysms

A

Clipping/ Coiling

39
Q

Treatments for

AVM

A

BP control

40
Q

Treatment of

Intracerebral Hemorrhage

A

BP control

41
Q

Treatment for

Subarachnoid hemorrhage

A

BP control

42
Q

Symptoms of

Intracerebral Hemorrhage

A

Focal signs, headache, nausea, confusion

43
Q

Symptoms of

Subarachnoid hemorrhage

A

Worst headache ever, stiff neck

44
Q

What is the first step in evaluating a patient with symptoms of stroke and what methods can be used to assess it?

A

The first step is to determine whether the stroke resulted from hemorrhage or infarct. Methods to assess this involve non-contrast CT (first choice), LP, CT/MRI angiography.

45
Q

How are hemorrhagic strokes treated?

A

Hemorrhagic strokes are treated by controlling blood pressure. Aneurysms can be clipped or coiled.

46
Q

What are some complications of these strokes?

A

Hemorrhage can result in hydrocephalus if ventricular blockage occurs and cerebral vasospasm due to irritability of blood, which can be treated with nimodipine.

47
Q

How does cerebral blood flow respond to changes in systemic arterial pressure?

A

CBF remains constant from 50 – 150 mmHg of systemic arterial pressure.

This ensures that the brain, which utilizes 20% of the energy output of the body, has adequate supply of O2 and glucose to function normally

48
Q

Explain

Excitotoxicity

A

Excitotoxicity occurs from exposure to low O2 levels/ischemia

49
Q

Explain

How ischemia causes excitotoxicity

A

Excitotoxicity occurs from exposure to low O2 levels/ischemia. Under this condition, oxidative metabolism is reduced and glycolysis is insufficient to produce enough ATP to maintain the Na/K pump. As a result, intracellular Na levels rise, cytotoxic edema occurs, electrical activity eventually ceases, the neurons depolarize, and glutamate is released from terminals. Glutamate binds to AMPA and NMDA postsynaptic receptors allowing prolonged Ca++ entry into neurons. The wave of intracellular Ca++ activates degradative proteins and free radicals.

50
Q

In which CNS locations are neurons most sensitive to ischemia ?

A

Hippocampus, cerebellum, cortex

IMC606: Neurology (11 decks)

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