CNS Flashcards

1
Q

neuronal injury can be an:

A

acute process

slower process

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2
Q

consequence of the depletion of oxygen, glucose or trauma

A

acute process

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3
Q

accumulation of protein aggregates, as occurs in degenerative disorders of the brain

A

slower process

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4
Q

refers to a spectrum of changes that accompany acute CNS hypoxia/ischemia

A

acute neuronal injury (red neuron)

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5
Q

earliest morphological marker of neuronal cell death

A

acute neuronal injury (red neuron)

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6
Q

red neuron is evident by about ____ hrs after an irreversible hypoxic /ischemic insult

A

12-24

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7
Q

morphologic features of red neuron

DILPS

A
disapperance of the nucleolus
intense eosinophilia of the cytoplasm
loss of nisl substance
pyknosis of the nucleus
shrinkage if the cell body
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8
Q

neuronal death as a result of a progressive disease of some duration

A

subacute and chronic neuronal injury (degeneration)

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9
Q

examples of subacute and chronic neuronal injury

A

amyotrophic lateral sclerosis and alzheimer’s disease

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10
Q

histologic features of subacute and chrinic neuronal injury

A

reactive gliosis

cell loss

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11
Q

best indicator of neuronal injury

A

reactive gliosis

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12
Q

changed observed in the cell body during regeneration of the axon

A

axonal reaction

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13
Q

axonal reaction is best seen in ________ of the spinal cord when motor axons are cut or seriousl damaged

A

anterior horn cells

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14
Q

classsic hallmark of axonal regeneration where there is increased protein synthesis associated with axonal sparring

A

central chromatolysis

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15
Q

most important histopathologic indicator of CNS injury characterized by both hypertrophy and hyperplasia of astrocytes

A

gliosis

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16
Q

a cell type specific intermediate filament

A

glial fibrillary acidic protein (GFAP)

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17
Q

T/F: astrocytes act as metabolic buffers and detoxifiers w/n the brain

A

true

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18
Q

T/F: astrocytes become gemistocytic astrocytes

A

true

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19
Q

Accumulation of excessive CSF within the ventricular system

A

Hydrocephalus

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20
Q

organ that produces CSF

A

Choroid Plexus

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21
Q

Production of CSF

A

Choroid Plexus —> lateral ventricle –> formaen of monroe–> third ventricle—> cerebral aqueduct of Sylvius—> Foramen of Magendie Luschka–> subarachnoid space—>arachnoid villi

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22
Q

Causes of Hydrocephalus

A

impaired flow and resorption of CSF

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23
Q

if hydrocephalus develops in infance before the closure of the suture os the head….

A

increase in the circumference of the head

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24
Q

if hydrocephalus develops after the closure of the sutures…

A

expansion of ventricles and increase in intercranial pressure

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25
Q

Types of Hydrocephalus

A

Communicating
Non-communicating
Hydrocephalus Ex Vacuo

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26
Q

Describe Non communicating hydrocephalus

A
  • only a portion is enlarged due to obstruction in the ventricular system
  • dies not communicate with the subarachnoid space
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27
Q

describe communicating hydrocephalus

A
  • has communication with the subarachnoid space

- enlargement of the entire ventricular system

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28
Q

dilation of the ventricular system with a compensatory increase in CSF volume secondary to a loss of brain parenchyma

A

Hydrocephalus Ex Vacuo

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29
Q

displacement brain tissue due to increase in intercranial pressure

A

Herniation

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30
Q

Explain Monroe-Kellie Doctrine

A

The CNS and its accompanying fluids are confined in one container whose total volume of one component will elevate pressure and decrease the volume of one of the other elements

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31
Q

Monroe-Kellie Equation

A

CCP=MAP-ICP

CCP- cerebral perfusion pressure
MAP= mean arterial pressure
=(systolic BP + 2 diastolic BP)/3
ICP=intracranial pressure

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32
Q

unilateral or asymmetric expansion of the cereral hemisphere that displace the cingulate gyrus under the falx that also causes impingement of the anterior cerebral artery

A

subfalcine herniation

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33
Q

medial temporal lobe compressed against the free margin of tentorium

A

transtentorial herniation

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34
Q

contralateral cerebral peduncle compression that reaults to he,iparesis of the contralateral side of the herniation

A

Kernohan’s notch

35
Q

secondary hemorrhagic lesions in midbrain and pons

these linear or flame-shaped lesions usually occur in the midline and paramedian regions

A

Duret hemorrhages

36
Q

displacement of cerebellar tonsils through foramne magnum

A

Tonsillar herniation

37
Q

T/F

Tonsillar herniation is not life-threatening at all.

A

False

if is life threatening because the brainstem it can compress the brainstem

38
Q

this malformation defects are due to failure to close or reopen a region in a neural tube

A

Neural tube defects

39
Q

diverticulum of a malformed brain tissue extending through a defect in the cranium

A

encephalocele

40
Q

Usually occurs in the posterior fossa, although comparable extensions of brain occur through the cribiform plate and the anterior fossa

A

encepahlocele

41
Q

failure of the closure of the posterior neuropore

A

spinal bifida

42
Q

Spina Bifida

asymptomatic body defect:
severe cord malformation:

A

Spina bifida; meningocoele

43
Q

Extension of the CNS tissue through a defect in the vertebral column that occur commonly in the lumbosacral region

A

myelomeningocele

44
Q

Failure of closure to the anterior neuropore

A

anencephaly

45
Q

other features of anencephaly

A

absence of brain and calvarium

flattened remnant of disorganized brain tissue

46
Q

enumerate posterior fossa anomalies

A

dandy-walker malformation
arnold-chiari malforamtion
chiari type 1 malformation

47
Q

characteristics of dandy walker malformation (CHEN)

A

cystic dilation of the fourth ventricle
hypoplasia of the cerebellar vermis
enlarged posterior fossa
non communicating hydrocephalus

48
Q

characterized as downward extension of cerebellar vermis through the foramen magnum; hydrocephalus; lumbar myelomeningocele

A

Arnold-Chiari Malformation

49
Q

low lying cerebellar tonsils extend down into the vertebral canal

A

Chiari type 1

50
Q

alterd consciousness secondary to head injury

A

concussions

51
Q

characteristic of concussions

A

loss of consciousness
loss of reflexes
temporary respiratory arrest

52
Q

caused transmission of KE to the brain

A

direct parenchymal injury

53
Q

differnce between contusion and laceration

A

contusion - bruise caused by blunt r
trauma
laceration- penetration of an object and tearing tissue

54
Q

occur at the site if the impact

A

coup injuries

55
Q

occur at the opposite side of the impact

A

contrecoup injuries

56
Q

yellowish brown patches that usually occurs at contrecoup injuries

A

Plaque jaune

57
Q

T/F

deep white matter regions of the brain are always safe from injuries

A

false

aside from the suface of the brain… white matter can also have traumatic injuries (diffuse axonal injury)

58
Q

epidural hematoma

A

arterial bleed which creates a blood-filled space between the bone and the dura

59
Q

T/F: in epidural hematoma, the dura separates from the inner surface
of the skull

A

TRUE

60
Q

in epidural hematoma there is a fracture in the ___________ where the______________ courses beneath

A

temporoparietal bone; middle meningeal artery

61
Q

shaoe of lesion in epidural hematoma

A

lenticular shaped lesion

62
Q

describe acute subdural hematoma

A
  • along the surface
  • brain is flattened
  • subarachnoid space is clear
63
Q

multiple episodes of repeat bleeding

A

chronic subdural hematoma

64
Q

epidural vs subdural

A
epidural 
-lentiform
-arterial 
-middle meningeal artery
subdural
-crescent
-venous
-bridging vein
65
Q

aka diffuse ischemic/hypoxic encephalopathy

A

global cerebral ischemia

66
Q

generalized reduction of cerebral perfusion

A

Global cerebral ischemia

67
Q

______ infarcts usually occur in the regions of the brain and spinal cord that lie at the most distal reaches of the arterial blood supply

A

border zone (watershed)

68
Q

Neuronal loss and gliosis are uneven, with preservation of some layers and destruction of other producing a layer in the cerebral neocortex

A

pseudolaminar necrosis

69
Q

infarction of a specific region within the distribution of a compromised vessel

A

focal cerebral ischemia

70
Q

focal cerebral ischemia may be due to:

A

vasculitis, embolization and thrombosis

71
Q

Diff white and red infarcts

A

white infarcts: reactive gliosis, red neuron and liquefactive necrosis
red infarcts: parallel to white infarcts but with extravasation and resorption of the blood

72
Q

development of small cavitary infarcts which resemble a lake-like space (lacunae)

A

lacunar infarcts

73
Q

occurence of lacunar infarcts im decreasing frequency

LTIDCP

A
lenticular nucleus
thalamus
internal capsule
deep white matter
caudate nucleus
pons
74
Q

rupture of small caliber penetrating vessels that leaves behind a slit-like cavity

A

slit hemorrhages

75
Q

clinicopathologic syndrome that arises in an individual with malignant hypertension

A

hypertensive encephalopathy

76
Q

most common cause of intraparenchymal hemorrhage

A

hypertension

77
Q

second most common cause of intraparenchymal hemorrhage

A

cerebral amyloid angiopathy

78
Q

minute aneurysms aka

A

charcot-bouchard microaneurysms

79
Q

most frequent cause of clinically significant subarachnoid hemorrhage

A

intracranial aneurysms

80
Q

most common type of intracranial aneurysms

A

saccral anuerysm

81
Q

most common demyelinating disease

A

multiple sclerosis

82
Q

most common cause of dementia

A

alzheimer’s disease

83
Q

clinical presentation of alzheimer’s disease

A

impairment of higher intellctual function

progressive disorientation, aphasia, memory loss