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NS2 Test 2 > Chapter 28 part 2 > Flashcards

Chapter 28 part 2 Flashcards

1
Q

Periventricular leukomalacia

A
  • infarcts in supratentorial periventricular white matter

- chalky yellow plaques–white matter necrosis and calcification

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2
Q

Multicystic encephalopathy

A
  • ischemic damage of white and gray matter

- destructive cystic lesions develop throughout hemispheres

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3
Q

ulegyria

A

-thinned out, gliotic gyri that occurs in perinatal ischemic lesions of cerebral cortex

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4
Q

status marmoratus

A
  • marble like appearance of deep nuclei when irregular myelination occurs
  • movement disorders
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5
Q

Physical forces associated with head injury may result in:

A
  • skull fractures
  • parenchymal injuries
  • vascular injuries
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6
Q

Displaced skull fractures

A

-fracture-bone is displaced into cranial cavity by a greater distance than the thickness of the bone

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7
Q

basal skull fracture

A
  • symptoms of lower CNS
  • orbital or mastoid hematomas
  • impact to occiput or sides of head
  • CSF discharge from nose or ear
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8
Q

diastatic fractures

A

cross sutures

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9
Q

concussion- characteristic neurological symptoms

A
  • instant onset of transient neurological dysfunction

- loss of consciousness, temporary respiratory arrest, loss of reflexes, amnesia of the event

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10
Q

coup injury

A

-point of contact

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11
Q

contrecoup injury

A

-impacts with the skull

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12
Q

concussion morphology

A
  • early stages–edema, hemorrhage
  • later- extravasation of blood
  • 24 hours–neuronal injury
  • old traumatic lesions–plaque jaune (depressed, retracted, yellowish brown patches)
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13
Q

Diffuse axonal injury–what indicates it?

A
  • surface of brain most affected

- axonal swelling!!!

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14
Q

Diffuse axonal injury morphology

A

axonal swelling–hours after injury

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15
Q

Hemorrhage can occur in?

A
  • Epidural
  • Subdural
  • Subarachnoid
  • Intraparenchymal
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16
Q

Epidural hematoma is caused by?

A
  • Middle meningeal a
  • Temporal skull fractures–trauma!!
  • dura separates from inner surface of skull
  • rapidly evolving symptoms
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17
Q

Subdural hematoma caused by?

A
  • bridging veins
  • accumulation of blood between dura and arachnoid
  • doesn’t have to be trauma!!
  • slowly evolving neurologic symptoms
  • older patients with brain atrophy–bridging veins are stretched
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18
Q

Acute subdural hematoma morphology

A
  • Lysis of clot- 1 week
  • growth of fibroblasts from dural surface into hematoma- 2 weeks
  • development of hyalanized CT (1-3 months)
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19
Q

Chronic subdural hematoma morphology

A

-recurrent episodes of bleeding occurs- from thin-walled vessels of granulation tissue

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20
Q

posttraumatic hydrocephalus is due to?

A

-obstruction of CSF resorption from hemorrhage into subarachnoid spaces

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21
Q

Chronic traumatic encephalopathy (CTE)

A
  • dementing illness after repeated head trauma
  • atrophic, enlarged ventricles, tau-containing neurofibrillary tangles
  • repeated concussions
22
Q

Spinal cord injury morphology

A
  • acute phase- hemorrhage, necrosis, axonal swelling

- in time- central areas of neuronal destruction becomes cystic and gliotic

23
Q

hypoxia vs. ischemia

A
  • hypoxia: low PO2, impairment of blood’s O2 carrying capacity
  • ischemia: interruption of normal circulatory flow
24
Q

biochemical changes in cells from ischemia

A
  • depletion of ATP
  • Ca levels elevated- act enzymes- cellular injury
  • inappropriate release of EAA NTs-binds to NMDA receptors-causes calcium influx
25
Q

penumbra

A

-at risk tissue- region of transition between necrotic tissue and normal brain

26
Q

Most sensitive neurons to ischemia

A
  • pyramidal cell layer of hippocampus (CA1- sommer sector)
  • cerebellar Purkinje cells
  • Pyramidal neurons in cerebral cortex
27
Q

Greatest risk for border zone (watershed) infarcts

A

-between anterior and middle cerebral artery

28
Q

Global cerebral ischemia morphology

A
  • early: eiosinophilia of neuronal cytoplasm, nuclear pyknosis
  • subacute: tissue necrosis, macrophage influx, vascular proliferation, reactive gliosis
  • repair: removal of necrotic tissue, gliosis
  • psudolaminar necrosis: preservation of some layers and destruction of others due to uneven neuronal loss and gliosis
29
Q

embolisms–from where? What is most affected?

A
  • cardiac mural thrombi–most common
  • thromboemboli arising in arteries- atheromatous plaques in carotid arteries
  • paradoxical emboli, cardiac surgery, emboli of other material
  • MCA and ICA most affected!!
30
Q

Infarcts– 2 groups based on presence of hemorrhage

A
  • begin with loss of blood supply and nonhemorrhagic

- secondary hemorrhage–occurs from ischemia-reperfusion injury- petechial

31
Q

non-hemorrhagic infarct-microscopic morphology

A
  • 12 hrs: ischemic neuronal change, vasogenic edema, glial cells swell
  • 48 hours-phagocytic cells
  • 1 week- reactive astrocytes
  • months: meshwork of glial fibers with new capillaries and perivascular CT
32
Q

4 most important effects of hypertension of brain

A
  • lacunar infarcts
  • slit hemorrhages
  • hypertensive encephalopathy
  • hypertensive intracerebral hemorrhage
33
Q

Lacunar infarcts

A
  • small cavitary infarcts
  • lakelike spaces, less than 15 mm wide
  • tissue loss surrounded by gliosis
34
Q

slit hemorrhages

A
  • rupture of small penetrating vessels and development of hemorrhages
  • hemorrhages resorb in time–leave a slitlike cavity surrounded by brownish discoloration
35
Q

hypertensive encephalopathy–what is it? caused by?

A
  • diffuse cerebral dysfunction–headaches, confusion, vomiting, convulsions, sometimes coma
  • malignant hypertension- over years suffer multiple infarcts
36
Q

intraparenchymal hemorrhage

A
  • rupture of small intraparenchymal vessel
  • sudden onset of neurologic symptoms
  • middle to late adult life
37
Q

risk factor most commonly associated with deep brain parenchymal hemorrhages

A
  • hypertension–>vessel wall abnormalities–atherosclerosis in large arteries, hyaline arteriosclerosis in smaller arteries, necrosis in severe cases
  • hyaline change in arteriolar walls- weaker, vulnerable to rupture
38
Q

carcot-bouchard microaneurysms

A
  • minute aneurysms- in vessels less than 300 um in diameter

- most commonly within basal ganglia

39
Q

hypertensive intraparenchymal hemorrhage–acute? old hemorrhage?

A
  • extravasation of blood with compression of adjacent parenchyma
  • central core of clotted blood–surrounded by a anoxic neuronal and glial changes and edema
  • macrophages
  • reactive astrocytes
  • old hemorrhage- cavitary destruction with rim of brownish discoloration
40
Q

risk factor most commonly associated with lobar hemorrhages? gene?

A
  • CAA (cerebral amyloid angiopathy)
  • amyloid peptides are deposited in walls of meningeal and cortical vessels- weakens the vessel wall-hemorrhage
  • polymorphism in gene that encodes ApoE
41
Q

CADASIL (cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy)- genes? characterized by?

A
  • autosomal dominant disorder
  • mutations in NOTCH3 gene- misfolding of NOTCH3- expression in vascular smooth muscle
  • recurrent strokes and dementia
42
Q

Most frequent cause of clinically significant subarachnoid hemorrhage?

A
  • rupture of a saccular (berry) aneurysm in a cerebral a

- 90% in anterior circulation

43
Q

rupture of aneurysm- subarachnoid hemorrhage clinical features

A
  • rupture of aneurysm- 5th decade of life
  • greater than 10mm- 50% risk of bleeding per year
  • occurs with acute increases in intracranial Pressure=straining at stool/ sexual orgasm
  • healing-meningeal fibrosis and scarring- can cause obstruction of CSF flow or resorption
44
Q

4 vascular malformations of the brain

A
  • arteriovenous malformations
  • cavernous malformations
  • capillary telangiectasias
  • venous angiomas
45
Q

arteriovenous malformations (AVM)

A

-tangled network of vascular channels-arteriovenous shunting!!!

46
Q

cavernous malformations

A

-dilated BVs that are characterized by multiple distended caverns of blood filled vasculature through which the blood flows very slowly

47
Q

capillary telangiectasias

A
  • dilated, thin walled vascular channels

- most common in pons!!

48
Q

venous angiomas (varices)

A

-characterized by an enlarged collection of veins which, other than their size, are microscopically normal

49
Q

Foix-Alajouanine disease

A

-arteriovenous malformation of spinal cord and meninges-associated with ischemic injury to spinal cord

50
Q

AVM (arteriovenous malformation)- clinical features

A
  • males=2X frequent
  • 10-30 years age- present as seizure disorder, intracerebral hemorrhage or subarachnoid hemorrhage
  • MCA most common site

NS2 Test 2 (16 decks)

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