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System Pathology I -- Roecker > Exam 2: CNS Pt1 > Flashcards

Exam 2: CNS Pt1 Flashcards

1
Q

What is the parenchyma of the CNS?

A

(functioning part)

- neurons and glial cells

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2
Q

T/F. CNS neurons are incapable of division and injury to theses cells in permanent.

A

True (but can have Reversibly injured neurons and Irreversibly injured neurons

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3
Q

What is the concept that occurs in the CNS where area/types of neurons that share similar levels of functionality, physical connections, NTs, or similar metabolic requirements are all prone to injury from similar pathological stimuli?

A

Selective vulnerability

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4
Q

How do Reversibly injured neurons manifest?

A
  • swelling of soma
  • “spheroids” (= swelling of axon)
  • “central chormatolysis” (= peripheral displacement of Nissl substance)
  • axonal sprouting
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5
Q

How does Irreversibly injured neurons manifest?

A
  • shrunken soma
  • nuclear pyknosis
  • eosinophilia
    ~all w/in 12-24 hrs
  • appear as small “red neurons” (‘red is dead’)
  • dissolution of nucleolus and Nissl substance
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6
Q

Would Reversibly or Irreversibly injured neurons manifest from times of acute hypoxia or sudden ischemia?

A

Irreversibly injured axons –> lead to inflammation and cause cerebral edema

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7
Q

Which cells of the CNS when injured manifest by hypertrophy, hyperplasia, and eosinophilia?

A

Astrocytes (astroglia)

- activation of them = gemistocytic astrocyte

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8
Q

Which cells of the CNS produce myelin and when injured hypertrophy and are usually infected by viruses?

A

Oligodendrocytes

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9
Q

Which type of CNS cell are the phagocytes of the CNS and after injury hypertrophy and hyperplasia occurs?

A

Microglia (“neurophagia”)

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10
Q

Which cells of the CNS line ventricles and spinal cord and commonly infected by CMV (cytomegalovirus)?

A

Ependymal cells

  • could be possible choroid plexus dysfunction (recall it produces CSF)
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11
Q

BOARDS: What are the key characteristics on how these manifest?

  1. Rabies
  2. CMV (cytomegalovirus)
  3. Parkinson Disease
  4. Alzheimer Disease
A
  1. Negri body
  2. owl’s eye appearance
  3. Lewy bodies
  4. Neurofibrillary tangles; beta-amyloid plaques (Tau proteins)
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12
Q

What is lipofuscin?

A

the lipid accumulation occurring with aging

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13
Q

What are 4 things that take up space and therefore may be a cause for injury?

A
  1. Blood
  2. Pus
  3. Tumor
  4. Edema
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14
Q

What are the two forms of cerebral edema?

A
  1. Vasogenic edema

2. Cytotoxic edema

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15
Q

Which type of cerebral edema develops when the BBB is disrupted and causes EXTRACELLULAR edema?

A

Vasogenic edema

- can be localized or generalized

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16
Q

What can disrupt the BBB and therefore cause vascogenic edema?

A

localized– tumor, inf. inflam.

generalized–trauma

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17
Q

Which type of cerebral edema causes INTRACELLULAR edema and develops when membranes of neurons and glial cells are injured?

A

Cytotoxic edema

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18
Q

What refers to an increase in CSF volume w/in the ventricular system? What are two ways this may occur?

A

Hydrocephalus

  1. increase production of CSF (via choroid plexus tumor or altered CSF flow)–rare
  2. reduced resorption of CSF at arachnoid granulaes
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19
Q

If hyrdocephalus develops proior to closure of cranial sutures around age 2, what occurs? What is it develops after the closure of the cranial sutures?

A

before–> head enlarges

after–> ventricles enlarge and severe increase in ICP

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20
Q

What percentage of hydrocephalus causes are known?

A

about 1/2; 50% are idiopathic

congenital (3 in 1,000 live births)

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21
Q

What describes a symmetrical enlargement of ventricular system and is most likely to be results of reduced CSF resorption?

A

Communicating hydrocephalus

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22
Q

What describes asymmetrical enlargement of the ventricular system (one area enlarged and the other normal)? What could this be due to?

A

Noncommunicating hydrocephalus

due to obstructed CSF flow –> tumore, gliosis, space-occupying lesion

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23
Q

What describes an increase in CSF volume that is secondary to loss of brain parenchyma from a pathological situation, such as a stroke or from advanced stages of neurodegenerative diseases?

A

Hydrocephalus ex vacuo

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24
Q

What is the MC cause of overproduction of CSF?

A

choroid plexus tumor

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25
Q

What involves a displacement of CNS tissues from its normal location in response to increase ICP?

A

Cerebral herniation

-typically across rigid dural structures or through foramen magnum

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26
Q

What will Cerebral herniations commonly cause?

A
  • sudden reduction of perfusion to herniated CNS tissue–> cause infarction–> which causes inflammation and edema –> increase ICP

(create positive feedback loop)

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27
Q

What are the three common cerebral herniations we are focusing on?

A
  1. Subfalcine (cingulate) herniation –MC
  2. Transtentorial (uncinate) herniation
  3. Tonsillar herniation
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28
Q

What is the MC type of cerebral herniation?

A

Subfalcine (cingulate) herniation

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29
Q

What type of herniation occurs when the cingulate gyrus herniates under the falx cerebri and superior to corpus callasum? What does this cause?

A

Subfalcine (cingulate) herniation

  • abnormal posturing –> decorticate rigidity
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30
Q

What type of abnormal rigidity involves brachial flexion, internal rotation of legs? Where does this injury occur b/w?

A

Decorticate Rigidity (“think cortex is higher and arms flex up”)

injury b/w cortex and red nuclei (midbrain)

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31
Q

What type of abnormal posturing involves all limbs extended and arms are pronated with flexed wrists? Where does this injury occur?

A

Decerebrate rigidity

brainstem–> b/w red nuclei and vestibular nuclei

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32
Q

What type of herniation occurs when the uncinate fasciculus of the temporal lobe herniates under the tentorium cerebelli?

A

Transtentorial (uncinate) Herniation

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33
Q

What type of herniation characteristically causes mydriasis (“blown pupil”) , diplopia,, hemiparesis and Duret hemorrhage?

A

Transtentorial (uncinate) Herniation

34
Q

What is anisocoria?

A

general term for unequal pupil size

35
Q

Describe a Duret hemorrhage.

A

“flame-shaped” hemorrhages (bleeds) w/in pons following a transentorial herniation

36
Q

What occurs when the cerebellar tonsils herniate through the foramen magnum?

A

Tonsillar Herniation

37
Q

What herniation characteristically causes brain stem compression and may cause dysregulation of cardiac or respiratory centers in medulla and could be lethal if compression is significant enough?

A

Tonsillar Herniation

38
Q

What are Chiari Malformations? What are they a common cause of?

A

a group of related congenital hindbrain abnormalities

common cause of Tonsillar herniaitons

39
Q

What are the two Chiari Malformations of our focus?

A
  1. Chiari Malformation Type I (=MC)

2. Arnold-Chiari Malformation (Type II)

40
Q

What is characterized by low-lying cerebellar tonsils combined with downward extension of cerebellar tonsils through foramen magnum?

A

Chiari malformation type I

41
Q

How will a Chiari malformation Type I manifest?

A

typically as a headache or neck pain (cervicalgia) during ADULThood

–more severe could create neurological abnorms and brain-stem compression

42
Q

T/F. Arnold-Chiari Malformation (Chiari malformation Type II) is less severe the Chiari Malformation Type I.

A

False- it is more severe

43
Q

Which type of Chiari malformation is most likely to be discussed in utero or shortly after birth? How does it manifest?

A

Arnold-Chiari Malformation (Chiari malformation Type II)

  • small posterior fossa
  • misshapen cerebellum
  • extension of malformed cerebellar tonsils through foramen magnum
44
Q

What may children experience that have Arnold-Chiari Malformation (Chiari malformation Type II)?

A
  • obstructive hydrocephalus
  • life-threatening brain stem compression
  • increased risk of having myelomeningocele
45
Q

What is the 5th MC cause of death in US and is the MC cause of neurologic morbidity?

A

Stroke (cerebral infarct)

46
Q

What is Cerebrovascular disease?

A

a pathology of the brain that is caused by variety of vascular pathologies; most likely results from hypoxia (lack of O2)

= Cerebrovascular accidents (CVA)

47
Q

What are risk factors for cerebrovascular disease (CVD)?

A
  • hypertension
  • atherosclerosis
  • smoking
  • diabetes
  • vasculitis
48
Q

What are the three main mechanisms that cause cerebrovascular disease (CVD)?

A
  1. thrombotic occlusion of vessel lumen
  2. embolic occlusion of vessel lumen
  3. disruption of vessel wall
49
Q

How is a stroke (cerebral infarction) defined?

A

death of CNS tissue following severe ischemia/hypoxia

50
Q

If a man over 50 comes in and has unilateral drooping of lower half of face, difficulty speaking/speaking nonsensical sentences, and difficulty coordinating motor movement, what are you thinking?

A

STROKE

  • may also have headahce, diplopia, or unilateral paralysis
51
Q

T/F. Cerebral infarction will cause paralysis of opposite side of body.

A

True–due to contralateral innervation of motor cortex

52
Q

What are the two primary forms of stroke?

A
  1. Ischemic Stroke

2. Hemorrhagic Stroke

53
Q

What develops following a lack of blood supply to an area of the brain due to a thromboembolism that occludes the central lumen of a cerebral artery?

A

Ischemic stroke

54
Q

Describe how a Hemorrhagic stroke manifests and how this type of injury in twofold.

A

disruption of cerebral vessel
1st–> injury CNS tissue b/c poor perfusion to CNS tissue
2nd—> disrupts BBB and have neurotoxic effect on neurons exposed

55
Q

What involves an acute onset of neurological dysfunction following a period of ischemia to CNS, but death of CNS tissues does not occur?

A

Transient Ischemic Attack (TIA)

56
Q

Some people call TIA’s a “mini stroke”, why is this misleading?

A

b/c TIA’s do NOT involve CNS tissue death, and strokes by definition cause CNS tissue death

57
Q

If someone could be having a stroke, what is a key word to remember what to do?

A 
FAST
F-- face dropping
A-- arm weakness
S-- speech difficulty
T-- time to call 911
58
Q

What are TIA’s defined as when it comes to restoration of neurological dysfunction?

A

restore neurological dysfunction w/in 24-hrs from time of onset

most resolute w/in minutes to hours

59
Q

What is the MC cause of unilateral facial paralysis?

A

Bell’s Palsy (aka idiopathic facial paralysis)

60
Q

What is defined as an acute unilateral paralysis of one entire side of the face, and cause is idiopathic?

A

Bell’s Palsy

61
Q

Even though Bell’s Palsy is idiopathic, what is frequently discovered in patients with Bell’s Palsy?

A

inflammation of CN VII

cause of inflammation is highly variable

62
Q

What are potential causes of facial nerve inflammation that could be ass. with Bell’s Palsy?

A
  • HSV-1 inf. (oral herpes)
  • mechanical traume
  • cold exposure
  • Lyme disease
  • mono (EBV) inf.
63
Q

T/F. Bell’s Palsy has a small familial ass. (4% all cases), but it is not well understood.

64
Q

How can you tell if someone is having a stroke or they have Bell’s Palsy? What about Bell’s Palsy makes it different than a stroke?

A
  • facial paralysis involves upper and lower portions of one side of face
  • unable to raise eyebrows/wrinkle forehead
  • unable to close eye
  • unable to make facial expression or move mouth on one side
65
Q

What are some additional features of Bell’s Palsy besides the main ones?

A
  • aching of ear or mastoid pain
  • altered taste
  • tingling or numbness in mouth
  • blurred vision
66
Q

How is Bell’s Palsy Dx?

A

by exclusion of more serious facial paralysis causes

67
Q

What age group is MC to get Bell’s Palsy? How is it Tx?

A

ages 15-45 years

~90% of Bell’s Palsy self-resolve w/in 2-8 wks

68
Q

What do we call it when the entire brain is not receiving adequate blood supply? What does this cause?

A

Global Cerebral ischemia

causes widespread (global) injury to brain and produces widespread edema and could involve widespread infarction

69
Q

What pathological states may Global Cerebral Ischemia may originate from?

A
  • severe hypertension (SBP <50 mm HG)
  • cardiac arrest
  • choking/strangulation
  • shock
70
Q

Global cerebral hypoxia may also cause Global cerebral ischemia, what may this originate from?

A
  • CO poisoning
  • severe anemia
  • cyanide poisoning
71
Q

If someone survives a Global cerebral ischemia incident, but neurologic disability occurs, like lasting motor and sesnory deficits, what can occur?

A

enter a coma

lose respiratory drive and enter vegetative state (lead to “respiratory brain”)

72
Q

What could being in a persistent vegetative state combined with long-term mechanical ventilation cause?

A

brain to initiate autolysis —> processes called “respirator brain”

73
Q

What MC causes a Focal Cerebral Ischemia?

A

due to embolism

74
Q

What manifests as occlusion of a cerebral artery creating a localized infarction, therefore isolated ischemia?

A

Focal Cerebral Ischemia

75
Q

What may cause a Focal Cerebral ischemia to occur?

A
  • (MC) embolism
  • cardiac mural thrombi (from heart attack)
  • cardiac valvular disease
  • atrial or ventricular fibrillation
    (anything creating turbulent blood flow)
76
Q

T/F. Embolic infarctions (causing Focal Cerebral Ischemia) can originate in venous system of a paradoxical embolism, and is more common.

A

False

statement is true, BUT is is RARE

77
Q

What is the most frequently affected area for an embolic occlusion to be detected, therefore causing Focal Cerebral Ischemia?

A

Middle cerebral artery

78
Q

T/F. Thrombotic occlusion is a less common cause of Focal cerebral ischemia, compared to the more common embolic occlusion.

A

True

  • thrombotic occlusions most likely develop atop atherosclerotic plaque in areas such as carotid arteries
79
Q

What type of cerebral infarct involves reperfusion of blood to site, terefore blood “pools” or collects in area of liquefactive tissue? What do these sites appear as?

A

Hemorrhagic infaracts

– “petechial hemorrhage”

80
Q

What type of cerebral infarcts do not involve reperfusion of blood to site of infarction? What do they appear like?

A

Nonhemorrhagiv infarcts

appear pale and liquefactive

81
Q

Regardless of the pattern of infarct, if the ind. survives, what cellular changes can we expect in the area? (3)

A
  1. Neutrophils, red neurons, edema (12-48 hrs)
  2. Nuclear fragmentation (karyorrhexis), liquefaction (48hrs-2wks)
  3. Macrophages and gliosis, cavitation (wks-years)

System Pathology I -- Roecker (14 decks)

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