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General Pathology > Pathology of the Central Nervous System > Flashcards

Pathology of the Central Nervous System Flashcards

1
Q

Three Primary CNS Diseases

A
  • Neural tube defects
  • Cerebral edema
  • Hydrocephalus
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2
Q

What are Neural tube defects (NTDs)?

A

a group of disorders characterized by failure of closure of the neural tube

(involve vertebrae and skull, w/ or w/o involvement of meninges, spinal cord, or brain)

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3
Q

What is notably increased with NTDs?

A

Concentration of alpha-fetoprotein (AFP) in amniotic fluid or maternal serum

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4
Q

What deficiency is associated with NTDs?

A

maternal folic acid

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5
Q

Six examples of NTDs

A
  • Spina bifida
  • Spina bifida occulta
  • Spina bifida cystica
  • Meningocele
  • Meningomyelocele
  • Anencephaly
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6
Q

Define Spina bifida

A

failure of posterior vertebral arches to close

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7
Q

Define Spina bifida occulta

A

spina bifida with no clinically apparent
abnormalities; defect limited to one
or two vertebrae

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8
Q

Define Spina bifida cystica

A

spina bifida complicated by herniation
of meninges through a defect

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9
Q

Define Meningocele

A

herniated membranes consisting of meninges
only

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10
Q

Define Meningomyelocele

A

portion of spinal cord included in
herniated tissue

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11
Q

Define Anencephaly

A

marked diminution (sometimes absence) of
fetal brain tissue; usually associated with the absence of overlying skull

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12
Q

73% of pts with spina bifida and related NTDs test positive for ___ ___ ___

A

hypersensitivity to latex

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13
Q

What is cerebral edema?

A

an abnormal accumulation of fluid in the
cerebral parenchyma

(results from BBB breakdown or damage)

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14
Q

What initiates damage resulting in cerebral edema? (x5)

A
  • Ischemia (infarction)
  • Trauma (head injury)
  • Inflammation encephalitis or meningitis
  • Cerebral tumors
  • Metabolic disturbances (hyponatremia or hypoglycemia)
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15
Q

Cerebral edema results in ___ ___ , and it is associated with raised ___ ___.

A

cerebral swelling, intracranial pressure

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16
Q

Cerebral edema treatment:

A

minimizing the formation of edema by use of:
- osmotic agents (mannitol)
- corticosteroids

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17
Q

What is hydrocephalus?

A

an increase in the volume of CSF within the
brain resulting in the expansion of the cerebral ventricles

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18
Q

Three mechanisms resulting in hydrocephalus:

A
  • Obstructive hydrocephalus; obstruction to the flow of CSF (most common)
  • Impaired absorption of CSF at arachnoid villi (rare)
  • Overproduction of CSF by choroid plexus neoplasms (very rare)
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19
Q

Obstructive hydrocephalus can be ___ or ___

A

congenital, acquired

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20
Q

Obstructive hydrocephalus is subdivided into:

A
  • Non-communicating hydrocephalus: obstruction within the ventricular system leading to blockage of CSF flow from the ventricles to the subarachnoid space.
  • Communicating hydrocephalus: extraventricular obstruction within subarachnoid space.
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21
Q

Five examples of traumatic brain injury:

A
  • Contusions
  • Concussions
  • Traumatic vascular injury
  • Epidural hematoma
  • Subdural hematoma
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22
Q

Define brain contusions

A

(parenchymal) contusion caused by rapid tissue
displacement, disruption of vascular channels, and subsequent hemorrhage, tissue injury, and edema.

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23
Q

Contusions occur ___ the site of impact and/or ___ ___ the site of impact

A

at, opposite to

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24
Q

Contusions at the site of impact are called ___ ___. Contusions opposite to the site of impact on the other side of the brain are called ___ ___.

A

coup injury, countercoup injury

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25
Q

Brain contusions morphology: shape

A

On cross-section, contusions are wedge-shaped, with the widest aspect closest to the point of impact

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26
Q

Brain contusions morphology: blood extravasation

A

Within a few hours of injury, blood extravasates throughout the involved tissue, across the width of the cerebral cortex, and into the white matter and subarachnoid spaces

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27
Q

Brain contusions morphology: evidence and function

A

Although functional effects are seen earlier, morphologic evidence of injury in the neuronal cell body (nuclear pyknosis, cytoplasmic eosinophilia, cellular disintegration) takes about 24 hours to appear

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28
Q

Brain contusions morphology: inflammatory response

A

follows usual course, with neutrophils preceding the appearance of macrophages

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29
Q

Define concussion

A

describes reversible altered consciousness from
head injury in the absence of contusion

(transient neurologic dysfunction)

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30
Q

Four characteristic of concussion

A
  • loss of consciousness,
  • temporary respiratory arrest
  • loss of reflexes
  • amnesia for the even (unknown pathogenesis)
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31
Q

What is traumatic vascular injury (TVI)?

A

CNS trauma often directly disrupts vessel walls, leading to hemorrhage

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32
Q

What does TVI classification depend on?

A

the affected vessel, the hemorrhage and hematoma formation

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33
Q

Four types of TVI

A
  • epidural
  • subdural
  • subarachnoid
  • intraparenchymal (intracerebral)
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34
Q

Epidural hematoma pathophysiology in infants vs. children and adults

A

Dural vessels (especially the middle meningeal artery) are vulnerable to traumatic injury:

  • In infants, traumatic displacement of the easily deformable skull may tear a vessel, even in the absence of a skull fracture.
  • In children and adults, by contrast, tears involving dural vessels almost always stem from skull fractures.
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35
Q

What can blood accumulation from a torn vessel result in?

A

under arterial pressure, it can dissect the tightly applied dura away from the inner skull surface producing a hematoma that compresses the brain
surface

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36
Q

What is the effect of an epidural hematoma on the patient?

A

Clinically, patients can be lucid for several hours between the moment of trauma and the development of neurologic signs

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37
Q

Epidural hematoma treatment and consequence

A

An epidural hematoma may expand rapidly and constitutes a neurosurgical emergency necessitating prompt drainage and repair to prevent death

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38
Q

What is subdural hematoma?

A

Rapid movement of the brain during trauma can tear the bridging veins that extend from the cerebral hemispheres through the subarachnoid and subdural space to the dural sinuses

39
Q

Which age groups are at risk of subdural hematomas?

A

Elderly and infants

40
Q

Pathophysiology of hematoma in elderly pts.

A

Bridging veins disruption produces bleeding into the subdural space.
Elderly patients with brain atrophy have a higher rate of subdural hematomas:
– The bridging veins are stretched out, and the brain has additional space within which to move,

41
Q

Pathophysiology of hematoma in infant pts.

A

Bridging veins disruption produces bleeding into the subdural space.
Infants are more susceptible to subdural hematomas because their bridging veins are thin-walled.

42
Q

When do subdural hematomas become clinically evident?

A

within the first 48 hours after injury

43
Q

Where are subdural hematomas most common?

A

over the lateral aspects of the cerebral hemispheres and may be bilateral

44
Q

Neurologic signs of subdural hematomas.

A
  • Attributable to the pressure exerted on the
    adjacent brain
  • Symptoms may be localizing but more often are
    nonlocalizing (headache, confusion, and
    slowly progressive neurologic deterioration)
45
Q

What is the treatment of symptomatic subdural hematomas?

A

surgical removal of the blood and associated reactive tissue

46
Q

Subdural hematomas commonly _____ during the healing process (resulting in ___ ___ ___).

A

rebleed, chronic subdural hematomas

47
Q

Subdural hematoma and underlying brain morphology

A
  • An acute subdural hematoma appears as a collection of freshly clotted blood apposed to the contour of the brain surface, without extension into the depths of sulci.
  • The underlying brain is flattened, and the subarachnoid space is often clear.
48
Q

Venous bleeding is self-limited with breakdown and organization of the hematoma taking place over time resulting in three morphological stages:

A
  • Subdural hematomas organize by lysis of the clot in about 1 week
  • growth of granulation tissue from the dural surface into the hematoma in about 2 weeks
  • fibrosis that occurs in 1 to 3 months

(Fibrosing lesions may eventually retract, leaving only a thin layer of connective tissue (“subdural membranes”).

49
Q

Define cerebrovascular disease (CVD)

A

injury to the brain as a consequence of altered blood flow

50
Q

What are the three types of CVD?

A
  • Cerebral infarctions
  • Intracerebral (Intraparenchymal) Hemorrhage
  • Subarachnoid Hemorrhage
51
Q

___ is the clinical designation that applies to all CVD conditions, particularly when symptoms begin acutely

A

Stroke

52
Q

What are the two possible mechanisms through which CVD develops?

A
  • Hypoxia, ischemia, and infarction
  • Hemorrhage
53
Q

Which is a amore common etiology in the brain, an embolism or a thrombosis?

A

An embolism, but occur

54
Q

Hypoxia, ischemia, and infarction can either be a ___ process or ___, with the clinical manifestations determined by the ___ of brain affected

A

global, focal, region

55
Q

Hemorrhage result from ___ of CNS vessels.

A

rupture

56
Q

Two common etiologies of hemorrhage include:

A
  • hypertension
  • vascular anomalies (aneurysms and malformations)
57
Q

Cerebral infarctions are most commonly caused by ___ ____ or ___ ___ ___ ___

A

Atherosclerotic thrombi, Emboli of cardiac origin

58
Q

Atherosclerotic thrombi are usually due to ___ ___ ___ ___ (___ ___), most commonly at the ___ ___

A

carotid artery atherosclerotic disease (plaque rupture), carotid bifurcation

59
Q

Emboli of cardiac origin are secondary to: (x3)

A

– valvular (especially, mitral valve) pathology
– acute anterior myocardial infarctions or congestive cardiomyopathies resulting in cardiac mural hypokinesias or akinesias with thrombosis
– cardiac arrhythmias (typically atrial fibrillation)

60
Q

The extent of a cerebral infarction is determined by: (x4)

A
  • site of the occlusion
  • size of the occluded vessel
  • duration of the occlusion
  • collateral circulation
61
Q

Neurologic abnormalities depend on: (x2)

A
  • the artery involved
  • its area of supply
62
Q

The gross appearance of an ischemic cerebral infarct varies with ___

A

time

63
Q

Describe the appearance of brain tissue effected by an infarction as time progresses

A
  • 1st 6 hrs of irreversible injury: there is little change in appearance
  • by 48 hrs: the tissue becomes pale, soft, and swollen, and the corticomedullary junction becomes indistinct.
  • from 2 to 10 ds: the brain becomes gelatinous and friable, and the previously ill-defined boundary between normal and
    infarcted tissue becomes more distinct as edema resolves in the viable adjacent tissue.
  • from 10 ds to 3 ws, the tissue liquefies (i.e.,
    liquefaction necrosis), eventually leaving a fluid-filled cavity that continues to expand until all of the dead tissue is removed.
64
Q

___ is the risk factor most commonly associated with clinically significant deep brain intracerebral (Intraparenchymal) hemorrhages

A

Hypertension

65
Q

Hypertension can cause vessel wall abnormalities (making them weaker and more vulnerable to rupture), including:

A
  • accelerated atherosclerosis in larger arteries,
  • hyaline arteriolosclerosis in smaller arteries,
  • proliferative changes and frank necrosis of
    arterioles (severe cases)
66
Q

Five locations where Hypertensive intraparenchymal hemorrhage can originate in:

A
  • putamen (50 - 60% of cases)
  • thalamus
  • pons
  • cerebellar hemispheres (rarely)
  • other regions of the brain
67
Q

Rupture of an artery within brain tissue leads to ___ of ___, which ___ ___ tissue and causes ___ intracranial volume until the resulting tissue ___ halts the bleeding

A

extravasation, blood, displaces brain, increased, compression

68
Q

What is the most frequent cause of clinically significant subarachnoid hemorrhage?

A

rupture of a saccular “berry” aneurysm in a cerebral artery

(most common type)

69
Q

___ ___ ___ is the most common type of intracranial aneurysm

A

Saccular (“berry”) aneurysm

(The vessels within the circle of Willis often are affected)

70
Q

Subarachnoid hemorrhage may also result from: (x4)

A
  • extension of a traumatic hematoma
  • rupture of a hypertensive intracerebral hemorrhage into the ventricular system
  • vascular malformation (e.g., arteriovenous malformation, cavernous malformation)
  • hematologic disturbances, and CNS tumors
71
Q

Name the eight infections CNS diseases

A
  • Bacterial Meningitis
  • Viral (Aseptic) Meningitis
  • Brain Abscess
  • Chronic Meningoencephalitis
  • Viral Encephalitis
  • Slow Virus Diseases
  • Fungal Infections
  • Protozoal Infections
  • Prion Diseases
72
Q

Meningitis is ___ of the meninges

A

inflammation

73
Q

Define Acute pyogenic (bacterial) meningitis

A

Infection of the leptomeninges (pia and arachnoid mater), and the CSF, which diffusely affects the whole meninges and subarachnoid space.

74
Q

What is the most serious form of meningitis?

A

Bacterial Meningitis

75
Q

Two organisms that cause Bacterial Meningitis are:

A

Neisseria meningitidis and Streptococcus pneumoniae

76
Q

What is the timeline of symptom development for bacterial meningitis?

A
  • About 25% have symptoms that develop over 24 hours
  • The remainder generally
    become ill over 1 to 7 days
77
Q

What are the classic symptoms of bacterial meningitis in adults? (x8)

A
  • headache
  • stiff neck (nuchal rigidity)
  • fever and chills
  • vomiting
  • photophobia
  • confusion
  • seizures (in ~ 33% of cases)
  • history of a recent upper respiratory infection
78
Q

Meningitis caused by ___ ___ may progress to a___ with multiple organ involvement, and may be associated with ___, petechial, or purpuric skin rash.

A

N. meningitidis, meningococcemia, maculopapular

79
Q

Meningococcemia is sometimes complicated by the ___ ___ syndrome

A

Waterhouse-Friderichsen

80
Q

What is Waterhouse-Friderichsen syndrome?

A

hemorrhagic destruction of the adrenal cortex, acute hypocorticism with circulatory collapse, and DIC

81
Q

Other complications of meningitis include: (x4)

A
  • ventriculitis,
  • intracerebral abscess
  • cerebral infarction
  • subdural empyema (a collection of pus in the subdural space)
82
Q

Diagnosis of bacterial meningitis:

A
  • CSF is cloudy due to increased numbers of neutrophils
  • CSF protein levels increase and
    glucose concentrations fall
83
Q

Treatment of bacterial meningitis:

A

vigorous intravenous antibiotic therapy

84
Q

prevention of bacterial meningitis:

A

a vaccine is available for meningitis caused by Neisseria meningitidis

85
Q

prognosis of bacterial meningitis:

A
  • mortality ranges from 3% for H. influenzae to 60% for Strep. pneumoniae
  • highest in the very young and
    the elderly
86
Q

Long-term complications of bacterial meningitis: (x9)

A

In addition to subtle CNS changes:
- nerve deafness
- cortical blindness
- paralysis
- muscular hypertonia
- ataxia
- complex seizure disorders
- learning disabilities
- obstructive hydrocephalus
- cerebral atrophy

87
Q

Three facts about viral (aseptic) meningitis:

A
  • the most common cause of meningitis. - it is a benign and self-limiting illness
  • less severe than bacterial meningitis
88
Q

Viral meningitis may occur as a ___ of viral infection, (e.g., ___ or ___)

A

complication, mumps, measles

89
Q

The two common causative organisms of viral meningitis are:

A
  • enteroviruses (e.g., echoviruses, coxsackie viruses, and polioviruses)
  • mumps virus (paramyxovirus)
90
Q

Symptoms of viral meningitis:

A

acute onset of:
- headache
- fever
- nuchal rigidity
- irritability
- rapid development of meningeal irritation

91
Q

Diagnosis of viral meningitis:

A
  • the CSF is clear and colorless
  • CSF contains excess lymphocytes, moderately increased protein, and normal glucose concentration
92
Q

Treatment of viral meningitis:

A

palliative care (control of symptoms) only

93
Q

Prognosis of viral meningitis:

A

Complete recovery usually occurs without specific therapy

94
Q
A

General Pathology (32 decks)

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