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NMSK Exam 2: Neuro > 28. CNS Pathology > Flashcards

28. CNS Pathology Flashcards

1
Q
A
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2
Q

Most common cerebrovascular diseases

A
  • 1. Hypertensive intraparenchymal hemorrhage (MC)
    1. Global ischemia
    1. Embolism
  • 4. Ruptured aneurism
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3
Q

When BF is reduced to the brain, survival depends on:

A
  • 1. Collateral flow
  • 2. Duration of ischemia (less than 24 hours = TIA; more than 24 hours = stroke)
  • 3. Magnitude and rapidity of flow reduction
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4
Q

Watershed areas 1st to be damaged to ischemia and infarction in global ischemia, because they are the most distal branches of major arteries.

In global cerebral ischemia or hypoxic encephalopathy, what type of damage do we see when watershed areas are affected?

A

Sickle-shaped band of necrosis

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5
Q
  1. Watershed areas 1st to be damaged to ischemia and infarction in global ischemia, because they are the most distal branches of major arteries. The border zone between which arteries in the cerebral hemispheres are most at risk for an infarct following global ischemia?
  2. What can cause this?
A

ACA/MCA

  1. Occlusion of the internal carotid artery
  2. Hypotension in patients with carotid stenosis
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6
Q

Symptoms if ischemia and infarction of ACA/MCA?

A
  1. Proximal arm and leg weakness.
  2. Transcortical aphasia: language problems
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7
Q

Symptoms if ischemia and infarction of MCA/PCA?

A
  1. Higher-order visual processing
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8
Q

Which pattern of injury is seen in the cerebral neocortex following global ischemia?

A

Pseudolaminar necrosis

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9
Q

Carotid Stenosis

  1. What is it?
  2. What is it most commonly due to?
A
  • Carotid stenosis is MC due to atherosclerosis. Thrombi can form and embolize, leading to stenosis of the internal carotid artery. This can ⬇︎ blood and O2 to the following arteries:
    • ​1. MCA
    • 2. ACA
    • 3. Opthalamic artery
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10
Q

What are symptoms of carotid stenosis?

A

Bc can ⬇︎ blood and O2 to the MCA, ACA and opthalamic artery =>

  1. Contralateral face-arm or face-arm leg motor/sensory weakness
  2. Contralteral changes in visual field
  3. Aphasia or neglect
  4. Carotid bruit in diastole
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11
Q

Carotid bruit heard in diastole is indicative of what?

A
  1. stenosis of internal carotid artery
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12
Q

How to correct carotid stensois?

A
  1. Angioplasty/stenting
  2. Endarterectomy
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13
Q

Focal cerebral ischemia, focal neurological deficits is most often due to what?

A
  1. Embolism
  2. Thrombus
  3. Atherosclerosis in HTN
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14
Q

Symptoms of Focal Cerebral Ischemia

A
  1. Less than 24 hours: TIA
  2. More than 24 hours: stroke (regional ischemia that causes focal neurological deficits)
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15
Q

Thrombosis

  1. MC due to: ______
  2. MC sites of primary thrombosis: ________
A
  1. Atherosclerosis
  2. MC sites of primary thrombosis:
    1. Carotid bifurcation
    2. origin of Middle Cerebral Artery (MC)
    3. Either end of the basialr artery
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16
Q

How does a thrombus form?

A
  1. Rupture, ulceration or erosion of plaque exposes blood to thrombogenic substances => blood is exposed to subendothelial collagen/necrotic debris in plaque => thrombus => pale wedge-shaped infarction at periphery of CTX
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17
Q

what is this?

A

subarachnoid hemorrhage: only thing that will cause bleeding at BOTTOM of brain

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18
Q

What is the risk factor most commonly associated with deep brain parenchymal hemorrhages?

A

HTN

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19
Q

What causes Charcot-Bouchard microaneurysms?

A

Chronic HTN

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20
Q

What is a Charcot-Bouchard microaneurysm vs. Saccular (berry) aneurysm?

Where is each most commonly seen?

A

- Charcot-Bouchard occur in vessels less than 300 um in diameter; most often within basal ganglia

- Saccular (berry) aneurysms occur in larger intracranial vessesl in the subarachnoid space

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21
Q

Intracerebral/ intraparenchymal hemorrhage vs subarachnoid hemorrage.

  • MC due to what?
  • MC seen in who?
  • Sx?
A

Intracerebral/intraparenchymal hemorrhage

  • MC due to: Rupture of Charcot Brousad microaneurysms (in pts who have HTN)
  • MC in: HTN patients
  • Sx: HA, N/V => coma

Subarachnoid hemorrhage

  • MC due to: R_upture of Berry/Saccular aneurysms_ in the Anterior Circle of Willis at the branch points of Anterior Communicating Artery; rupture easily bc no media
  • MC in: Marfans and APKD (bc they’re more likely to have berry aneuryms)
  • Sx: Worse HA of life with nuchal rigidity
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22
Q

What is most commonly affected by a embolic infarction?

Where do emboli most often lodge?

A
  1. L side of heart => Middle cerebral artery (MCA)
  2. Where BV branch of pre-existing areas of stenosis
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23
Q

What is characteristic of bone marrow embolization?

A
  1. Shower hemorrhages = widespread white matter hemorrhages
24
Q

What are heritable coagulation factor disorders that cause hypercoagulability?

A
  1. Protein S and C defiency
  2. Antithrombin III deficiency
25
Q

What are hypercoagulable states?

A
  1. Dehydration
  2. Adenocarcinomas/malignancies
  3. Surgery, trauma, childbirth
  4. DIC
  5. Hematologic disorders (sickle cell, leukemia, polycythemia)
26
Q

Symptoms in ischemic strokes vs hemorrhagic strokes take how long to come about?

A

Ischemic stroke = over 2 hours

Hemorrhagic = immediately

27
Q

MCC of TIA

A

1. Thrombi

2. Embolism

3. Vasospasm

or anything causing a blockage

28
Q

How should a patient with a TIA be treated?

A

Evaluate immediately for treatable causes of ischemic cerebrovascular disease: emboli, thrombus or vasospasm

29
Q

Hemorrhagic strokes are red because we usually get reperfusion. Ischemic event damages vessel => blood comes back in after it opens up => leaks inside the brain

Ischemic stokes can lead to hemorrhagic conversion: fragile vessels rupture => secondary hemorrhage.

A
30
Q

What are the four main injuries due to effects of hypertension on the brain?

A
  1. Lacunar infarcts (lacunar means small)
  2. Slit hemorrhages
  3. Acute hypertensive encephalopathy
  4. Hypertensive intracerebral hemorrhage
31
Q

Lacunar Infarcts/Lacunar Strokes

  • What are they caused by?
  • What are they?
  • Where do they occur?
  • SX?
A
  • Lacunar infarcts occur in people with HTN
  • HTN => Arteriolosclerosis of lenticulostriate arteries, which are branches of the Middle Cerebral Artery that provide blood to the deep parenchyma of the brain (thalmus, BG, internal capsule, deep white matter) => multiple small (<15mm) cavitary infarcts called lacunes in the (thalmus, BG, internal capsule, deep white matter)
  • Sx
    • Thalamus => contalateral somatosensory deficits
    • BG: hemiballismus
32
Q

Other HTN Cerebrovascular Disease?

A

1. Vascular multi-infarct dementia

2. Binswanger Disease

3. Charcot Brousard Microaneuryms

  1. CAA (Cerebral Amyloid Angiopathy)
  2. CADASIL (Cerebral AD Arteriopathy with Subcortical Infarcts and Leukoencephalopathy)
33
Q

What are slit hemorrhages?

A
  • HTN => small veins to repture, which resorb overtime and leave slit-like cavities surrounded by hemosidering MO and gliosis.
34
Q

What is acute HTN encephalopathy?

A

Clinicopathologic syndrome caused by malignant HTN.

  1. Edema in brain with or without transtenrotial or tonsillar herniation
  2. Petechaie and fibrinoid necrosis in arterioles in the grey and white matter
35
Q

Symptoms of vascular mulit-infarct dmentia?

A
  1. Dementia
  2. Gait abnormalities
  3. Pseudobulbar signs
36
Q

Binswanger Disease

A

Vascular dementias due to infarcts in only white matter (loss of myelin and axons)

37
Q

Charcot-Bouchard microaneurysms

A

Microaneurysms that occur due to chronic HTN in the BG and are the MCC of intraparenchymal hemorrhage

38
Q

CAA (Cerebral Amyloid Angiopathy)

MC in?

A
  • B-amyloid plaques that deposit in the walls of the artery after recurrent hemorrhagic strokes, making them weak and prone to rupture ==> microbleeds
  • Older patients and Alz (same AB amyloid)
39
Q

CADASIL (Cerebral AD Arteriopathy with Subcortical Infarcts and Leukoencephalopathy)

First detected?

A
  1. Rare cause of recurrent strokes and dementia due to mutations in NOTCH3 gene, expressed in vascular smooth muscles ==> thickening of media and adventitia, loss of smooth muscle cells and basophilic PAS+ deposits
  2. First detectable at 35 YO, however infarcts typically occur 10-15 year later in other cases
40
Q

RF for a stroke

A
  1. HTN
  2. DB
  3. Hypercholesterolemia
  4. Cigarrette smoking
  5. Cardiac Disease (Valvular, a-fib, PFO)
41
Q

What histological findings are common with age and represent a DEGENERATION of astrocytes?

A

Corpera amylcia: PAS+, intracytoplasmic, lamellated polyglucasan bodies; also have HSP

42
Q

markers of microglia

A

CR3

CD86

43
Q

AVMs are MC where and in whom?

A

Subarachnoid space => deep parenchyma

M 10-30 YO

44
Q

AVMs can cause what

A

intracerebral or SAH;

damage starts on surface of brain => deeper

45
Q

Neural tube defects are MC assx with what?

A
  1. T1DM/obesity
  2. Folic acid def
46
Q

Microcephaly is associated with

A

hiv

zika

FAS

47
Q

neuronal heterotropias are due to?

assoociated with

A

mutations on genes on x chr: DCX and filamin A

epilepsy

48
Q

when does holoproscencephly occur

ass w

A

5-6 weks due to SHH signaling

FAS, trisomy 13 and 18

49
Q

small posterior fossa and hernitation of cerebellum into foramen magnum

A

Chiari

50
Q

Chiari type 1

what herniates

MC in who

A

cerebellar tonsils

asx in childhood; sx in adulthood due to obstructive hydrocephalys and cerebellar sx (ataxia

51
Q

chiari type 1 malf is assx with

A

syringomyelia: bilateral loss of pain and temp in UE

52
Q

chiari type 2 is assx with

A

lumbosacral myelomeningecele (=paralysis/sensory loss below level of lzn)

53
Q

what do you see in chiari type 2 malform

A

herniation of tonsils AND vermis

aqueductal stenosis

54
Q

syringomyelia presents when

A

20-30s

55
Q

dandy walker malformation

A

huge posterior fossa

no cerebellum vermis

enlarged roofless 4th ventricle => cyst in posterior fossa

-pushes up on tentorium => obstructive hydrocephalus

56
Q

joubert syndrome

A
  1. Hypoplasia of vermis
  2. Lengthing of superior cerebral peduncles => molar tooth signs
  3. altered brainstemp shape

NMSK Exam 2: Neuro (15 decks)

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