Exam 2: CNS Pt1 Flashcards

(81 cards)

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
What involves a displacement of CNS tissues from its normal location in response to increase ICP?
Cerebral herniation -typically across rigid dural structures or through foramen magnum
26
What will Cerebral herniations commonly cause?
- sudden reduction of perfusion to herniated CNS tissue--> cause infarction--> which causes inflammation and edema --> increase ICP (create positive feedback loop)
27
What are the three common cerebral herniations we are focusing on?
1. Subfalcine (cingulate) herniation --MC 2. Transtentorial (uncinate) herniation 3. Tonsillar herniation
28
What is the MC type of cerebral herniation?
Subfalcine (cingulate) herniation
29
What type of herniation occurs when the cingulate gyrus herniates under the falx cerebri and superior to corpus callasum? What does this cause?
Subfalcine (cingulate) herniation - abnormal posturing --> decorticate rigidity
30
What type of abnormal rigidity involves brachial flexion, internal rotation of legs? Where does this injury occur b/w?
Decorticate Rigidity ("think cortex is higher and arms flex up") injury b/w cortex and red nuclei (midbrain)
31
What type of abnormal posturing involves all limbs extended and arms are pronated with flexed wrists? Where does this injury occur?
Decerebrate rigidity brainstem--> b/w red nuclei and vestibular nuclei
32
What type of herniation occurs when the uncinate fasciculus of the temporal lobe herniates under the tentorium cerebelli?
Transtentorial (uncinate) Herniation
33
What type of herniation characteristically causes mydriasis ("blown pupil") , diplopia,, hemiparesis and Duret hemorrhage?
Transtentorial (uncinate) Herniation
34
What is anisocoria?
general term for unequal pupil size
35
Describe a Duret hemorrhage.
"flame-shaped" hemorrhages (bleeds) w/in pons following a transentorial herniation
36
What occurs when the cerebellar tonsils herniate through the foramen magnum?
Tonsillar Herniation
37
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?
Tonsillar Herniation
38
What are Chiari Malformations? What are they a common cause of?
a group of related congenital hindbrain abnormalities common cause of Tonsillar herniaitons
39
What are the two Chiari Malformations of our focus?
1. Chiari Malformation Type I (=MC) | 2. Arnold-Chiari Malformation (Type II)
40
What is characterized by low-lying cerebellar tonsils combined with downward extension of cerebellar tonsils through foramen magnum?
Chiari malformation type I
41
How will a Chiari malformation Type I manifest?
typically as a headache or neck pain (cervicalgia) during ADULThood --more severe could create neurological abnorms and brain-stem compression
42
T/F. Arnold-Chiari Malformation (Chiari malformation Type II) is less severe the Chiari Malformation Type I.
False- it is more severe
43
Which type of Chiari malformation is most likely to be discussed in utero or shortly after birth? How does it manifest?
Arnold-Chiari Malformation (Chiari malformation Type II) - small posterior fossa - misshapen cerebellum - extension of malformed cerebellar tonsils through foramen magnum
44
What may children experience that have Arnold-Chiari Malformation (Chiari malformation Type II)?
- obstructive hydrocephalus - life-threatening brain stem compression - increased risk of having myelomeningocele
45
What is the 5th MC cause of death in US and is the MC cause of neurologic morbidity?
Stroke (cerebral infarct)
46
What is Cerebrovascular disease?
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
What are risk factors for cerebrovascular disease (CVD)?
- hypertension - atherosclerosis - smoking - diabetes - vasculitis
48
What are the three main mechanisms that cause cerebrovascular disease (CVD)?
1. thrombotic occlusion of vessel lumen 2. embolic occlusion of vessel lumen 3. disruption of vessel wall
49
How is a stroke (cerebral infarction) defined?
death of CNS tissue following severe ischemia/hypoxia
50
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?
STROKE - may also have headahce, diplopia, or unilateral paralysis
51
T/F. Cerebral infarction will cause paralysis of opposite side of body.
True--due to contralateral innervation of motor cortex
52
What are the two primary forms of stroke?
1. Ischemic Stroke | 2. Hemorrhagic Stroke
53
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?
Ischemic stroke
54
Describe how a Hemorrhagic stroke manifests and how this type of injury in twofold.
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
What involves an acute onset of neurological dysfunction following a period of ischemia to CNS, but death of CNS tissues does not occur?
Transient Ischemic Attack (TIA)
56
Some people call TIA's a "mini stroke", why is this misleading?
b/c TIA's do NOT involve CNS tissue death, and strokes by definition cause CNS tissue death
57
If someone could be having a stroke, what is a key word to remember what to do?
``` FAST F-- face dropping A-- arm weakness S-- speech difficulty T-- time to call 911 ```
58
What are TIA's defined as when it comes to restoration of neurological dysfunction?
restore neurological dysfunction w/in 24-hrs from time of onset most resolute w/in minutes to hours
59
What is the MC cause of unilateral facial paralysis?
Bell's Palsy (aka idiopathic facial paralysis)
60
What is defined as an acute unilateral paralysis of one entire side of the face, and cause is idiopathic?
Bell's Palsy
61
Even though Bell's Palsy is idiopathic, what is frequently discovered in patients with Bell's Palsy?
inflammation of CN VII cause of inflammation is highly variable
62
What are potential causes of facial nerve inflammation that could be ass. with Bell's Palsy?
- HSV-1 inf. (oral herpes) - mechanical traume - cold exposure - Lyme disease - mono (EBV) inf.
63
T/F. Bell's Palsy has a small familial ass. (4% all cases), but it is not well understood.
true
64
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?
- 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
What are some additional features of Bell's Palsy besides the main ones?
- aching of ear or mastoid pain - altered taste - tingling or numbness in mouth - blurred vision
66
How is Bell's Palsy Dx?
by exclusion of more serious facial paralysis causes
67
What age group is MC to get Bell's Palsy? How is it Tx?
ages 15-45 years ~90% of Bell's Palsy self-resolve w/in 2-8 wks
68
What do we call it when the entire brain is not receiving adequate blood supply? What does this cause?
Global Cerebral ischemia causes widespread (global) injury to brain and produces widespread edema and could involve widespread infarction
69
What pathological states may Global Cerebral Ischemia may originate from?
- severe hypertension (SBP <50 mm HG) - cardiac arrest - choking/strangulation - shock
70
Global cerebral hypoxia may also cause Global cerebral ischemia, what may this originate from?
- CO poisoning - severe anemia - cyanide poisoning
71
If someone survives a Global cerebral ischemia incident, but neurologic disability occurs, like lasting motor and sesnory deficits, what can occur?
enter a coma lose respiratory drive and enter vegetative state (lead to "respiratory brain")
72
What could being in a persistent vegetative state combined with long-term mechanical ventilation cause?
brain to initiate autolysis ---> processes called "respirator brain"
73
What MC causes a Focal Cerebral Ischemia?
due to embolism
74
What manifests as occlusion of a cerebral artery creating a localized infarction, therefore isolated ischemia?
Focal Cerebral Ischemia
75
What may cause a Focal Cerebral ischemia to occur?
- (MC) embolism - cardiac mural thrombi (from heart attack) - cardiac valvular disease - atrial or ventricular fibrillation (anything creating turbulent blood flow)
76
T/F. Embolic infarctions (causing Focal Cerebral Ischemia) can originate in venous system of a paradoxical embolism, and is more common.
False statement is true, BUT is is RARE
77
What is the most frequently affected area for an embolic occlusion to be detected, therefore causing Focal Cerebral Ischemia?
Middle cerebral artery
78
T/F. Thrombotic occlusion is a less common cause of Focal cerebral ischemia, compared to the more common embolic occlusion.
True - thrombotic occlusions most likely develop atop atherosclerotic plaque in areas such as carotid arteries
79
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?
Hemorrhagic infaracts -- "petechial hemorrhage"
80
What type of cerebral infarcts do not involve reperfusion of blood to site of infarction? What do they appear like?
Nonhemorrhagiv infarcts appear pale and liquefactive
81
Regardless of the pattern of infarct, if the ind. survives, what cellular changes can we expect in the area? (3)
1. Neutrophils, red neurons, edema (12-48 hrs) 2. Nuclear fragmentation (karyorrhexis), liquefaction (48hrs-2wks) 3. Macrophages and gliosis, cavitation (wks-years)