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System Pathology I -- Roecker > Exam 2: CNS Pt2 > Flashcards

Exam 2: CNS Pt2 Flashcards

1
Q

What is the general term for bleeding that occurs within the skull?

A

intracranial hemorrhage

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2
Q

What are the 4 intracranial hemorrages we are covering?

A
  1. Primary Brain Parenchymal Hemorrhage
  2. Subarachnoid Hemorrhage (saccular aneurysm)
  3. Ruptured AVM
  4. Lacunar Infarct and Slit Hemorrhage
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3
Q

Causes of intracranial hemorrhage are widely variable. Name some of the possible causes:

A
  • long-term hypertension
  • trauma
  • vascular malformations
  • intracranial tumors
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4
Q

What is a spontaneous (nontraumatic) form of intracranial hemorrhage that is most likely to occur in older adults around age 60 who have a history of long-term hypertension?

A

Primary Brain Parenchymal Hemorrhage

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5
Q

Are Primary Brain Parenchymal Hemorrhage small or large?

A

small, and sometimes referred to as “micro bleeds”—> but could develop into massive bleeds

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6
Q

T/F. Primary Brain Parenchymal Hemorrhage features are variable, but smaller hemorrhage, less likely to cause clically sig. features, and larger the hemorrhage, more life-threatening or lethal it may be.

A

True

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7
Q

What is the MC cause of Primary Brain Parenchymal Hemorrhage?

A

hypertension

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8
Q

About how many inds. with long-term hypertension die following Primary Brain Parenchymal Hemorrhage?

A

15%

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9
Q

If someone comes into your office and says “this is the worst headache I’ve ever had”, what are you thinking?

A

Subarachnoid hemorrhage–> medical emergency!!!

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10
Q

What occurs when bleeding exists w/in the subarachnoid space?

A

subarachnoid hemorrhage

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11
Q

What are subarachnoid hemorrhages characteristically associated with? But what else could cause them?

A

ruptured saccular aneurysms

  • ruptured intracranial vascular malformations or tissue distortion from benign or malignant intracranial tumor
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12
Q

What represents 90% of all intracranial aneurysms? Where are they most likely to develop?

A

Saccular aneurysms (AKA berry aneurysms)

–from anterior vessels of Circle of Willis, particularly at branched points

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13
Q

What percentage chance of rupturing each year do:
Saccular aneurysms smaller than 1 cm?
Larger than 1 cm?

A

smaller–> 1% chance

larger –> 50% chance

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14
Q

Are subarachnoid hemorrhages highly lethal?

A

yes! about 25-50% of all first-time bleeds results in death

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15
Q

What percentage of people that have one saccular aneurysm, have multiple?

A

about 30%

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16
Q

What are 6 of the most common risk factors someone may have that may be indicative of a subarachnoid hemorrhage?

A
  1. older than age 40
  2. “thunderclap” HA that peaks in intensity
  3. onset of HA with exertion
  4. loss of consciousness
  5. neck pain/stiffness (nuchal rigidity)
  6. limited neck flexion
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17
Q

What disease is ass. with intracranial saccular aneurysms on the Circle of Willis?

A

Polycystic Kidney Disease

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18
Q

What involves the bilateral formation of multiple cysts on the kidneys?

A

Polycystic Kidney Disease (PCKD or autosomal dominant polycystic kidney disease)

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19
Q

How do the cysts manifest in Polycystic Kidney Disease?

A

cysts expand as one ages and cause tissue ischemia, atrophy, and kidney failure

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20
Q

How common is Polycystic Kidney Disease? What is responsible for it?

A

1 in 500-1000 inds

90% have mutated PKD1 gene
other 10% have mutated PKD2 gene

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21
Q

What are common features of Polycystic Kidney Disease?

A
  • flank pain
  • a “dragging” or “heavy” sensation in area of kidneys
  • HAs
  • increased UTIs
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22
Q

When does Polycystic Kidney Disease manifest with clinically sig. features? When does end-stage kidney failure usually occur?

A

the 30s

the 50s

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23
Q

What other issues is Polycystic Kidney Disease associated with?

A
  • saccular aneurysms on Circle of Willlis

- multiple hepatic cysts

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24
Q

Saccular aneurysms are present in about ___ individuals with Polycystic Kidney Disease

A

30%

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25
Q

What is a tangled mass of arteries and veins that may develop anywhere w/in brain that involve tortuous vessels that manifest with telangiectasia and frequently contain a fistula?

A

Ateriovenous malformation (AVM)

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26
Q

What is a fistula?

A

an abnormal connection b/w large artery and large vein

cause nutrient rich blood to bypass capillary network

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27
Q

What are the most dangerous form of intracranial vascular malformation? What does it increase the risk of?

A

Ateriovenous malformation (AVM)

increased risk of intracranial hemorrhage

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28
Q

What is telangiectasia?

A

a cluster of widened vessels; superficial ones are referred to as “spider veins”

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29
Q

At what age and in what sex are Ateriovenous malformation (AVM) most likely to be discovered?

A

males b/w ages 10-30

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30
Q

What is present in about half of all cases of Ateriovenous malformation (AVM)? What else could AVMs cause?

A

headaches

Also:

  • subarachnoid hemorrhage
  • seizures
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31
Q

What percentage of Ateriovenous malformation (AVM) will rupture and cause a subarachnoid hemorrhage?

A

~4%

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32
Q

What may children develop that are born with large Ateriovenous malformation (AVM)?

A

high-output heart failure b/c of nutrient rich blood bypassing capillaries via presence of large fistula or mult.

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33
Q

What occurs when diastolic blood pressure is maintained at a level that is above 130 mm Hg?

A

Hypertensive encephalopathy (AKA acute hypertensive encephalopathy)

34
Q

What does Hypertensive encephalopathy cause?

A

disrupts BBB and produces widespread vasogenic edema–> which will increase ICP and glocal cerebral dysfunction

35
Q

What are some early indications of Hypertensive encephalopathy? If PB is NOT reduced, what can occur?

A
  • HA
  • confusion
  • vomiting

NOT reduced:

  • convulsions
  • coma
  • death
36
Q

T/F. Hypertensive encephalopathy is not a medical emergency.

A

FALSE– it is, and reducing BP is essential for survival

37
Q

What will individuals who end up dying from Hypertensive encephalopathy manifest with?

A
  • widespread cerebral edema
  • cerebral herniations
  • cerebral petechiae
  • fibroid necrossi in walls of cerebrum
38
Q

When it comes to CNS trauma, are males or females MC to get it?

A

males are 2x MC (violence, fights, MVA)

39
Q

What is a neurodegenerative pathology that develops from repetitive CNS trauma and manifest in a gradual onset?

A

Chronic Traumatic Encephalopathy (CTE, dementia pugilistica, or being “punch drunk”)

40
Q

What inds. is Chronic Traumatic Encephalopathy (CTE) MC reported in?

A
  • boxers
  • American Football players
  • inds with military history and have exposure to blast injuries
41
Q

What are some symptoms of Chronic Traumatic Encephalopathy (CTE)?

A
  • memory loss
  • aggressive changes in behavior/mood
  • increased impulsivity
  • depression
  • apathy
  • substance abuse
  • motor dysfunction
42
Q

How do we Dx Chronic Traumatic Encephalopathy (CTE)?

A

Dx is done post-mortem via detection of tau proteins in the brain (specifically p-tau proteins)

43
Q

What do we are clinicians need to keep in mind for a CNS trauma?

A 
ABCDs:
A- Airway
B- Breathing
C- Circulation
D- disability
44
Q

What is a Cerebral Contusion?

A

a contusion (blood vessels rupture and blood accumulates) develops in brain following trauma to brain and involves hemorrhagic CNS injury localized edema at the site

45
Q

What structure is the most susceptible to injury from Cerebral contusion? How does it manifest? What lobes are MC?

A

gyri

“wedge-shaped” with widest area near area of impact near skull

frontal lobe and temporal lobe

46
Q

What is a coup injury vs and contrecoup injury?

A

coup injury = contusion at side of injury

contrecoup injury = contusion occurs opposite side of brain as the impact

47
Q

What will occur when the brain suffers a penetrating wound, such as occurs with bullet wound or skull fragment entering the brain?

A

Cerebral laceration

laceration = wound that develops following tearing of a tissue following a trauma

48
Q

What will Cerebral lacerations injury? What will they cause?

A

neurons and glial cells and will cause hemorrhage via vascular disruption

hemorrhage–> could be epidural, subdural, or subarachnoid

49
Q

What describes widespread injury to the white matter of the deep brain tissues due to severe head trauma involving angular acceleration?

A

Diffuse axonal injury (DAI)

  • widespread axonal injury and edema
50
Q

T/F. Diffuse axonal injury (DAI) is rarely lethal.

A

FALSE–it is highly-lethal and involves severe neurological impairment

51
Q

What is responsible for half of all post-traumatic concussions?

A

Diffuse axonal injury (DAI)

52
Q

What is Shaken Baby Syndrome?

A

result of child abuse involving the forceful shaking of a child

(=non-accidental head injury or abusive head trauma)

53
Q

What do most cases of Shaken baby syndrome involve? Who else can experience it?

A

infants = MC

but children up to 5 years could experience it

54
Q

What are the three criteria for Shaken Baby Syndrome?

A
  1. Subdural hematoma
  2. Widespread cerebral edema
  3. Bilateral retinal hemorrhage
55
Q

Victims of Shaken Baby Syndrome may also have what ass.?

A

up to 95% have skull Fx ass.–> MC in occipital or parietal bones

56
Q

What percentage of Shaken Baby syndrome cases are lethal? What about the other 75%?

A

25%

75% survival will involve permanent neurological disability–> blindness, motor impairment (ataxia or cerebral palsy), and reduced cognitive functioning

57
Q

What is a concussion defined as?

A

form of brain injury involving temporary neurologic dysfunction following trauma

(mild traumatic brain injury, mTBI)

58
Q

We don’t know for sure what causes a concussion, but what is there preliminary evidence of? (4)

A
  1. reduced metabolic state
  2. dysregulated neurotransmission
  3. calcium and potassium ion imbalances
  4. reduced CSF flow rates
59
Q

What are common signs and symptoms of concussions?

A
  • HAs
  • neck pain
  • reduced cognition
  • disorientation
  • “in a fog”
  • loss of consciousness
  • nausea/vomiting
  • dizziness/ balance problems
  • ringing in ears (tinnitus)
  • photophobia and phonophobia
  • depression
  • fatigue
  • diplopia
  • difficulty sleeping
  • nervousness
60
Q

How do we Dx concussions?

A

cannot be objectively Dx

- Neurocognitive Testing –> SCATs or computerized ImPACT tests

61
Q

What is the term used to describe when inds experience persitent features of a concussion after a period of time where it reasonably should have been resolved (wk or months)?

A

Post-concussive syndrome

62
Q

How common is Post-concussive syndrome?

A

about 15% of all cases of concussion

63
Q

What is Second-impact syndrome?

A

develops when an ind. experiences a second concussion, BEFORE symptoms of earlier one were resolved

64
Q

The mechanisms of Second-impact syndrome are not understood, but what is it thought to cause it?

A

thought that the 2nd concussion causes dysregulation of intracranial arterioles–> thus causing widespread intracranial edema

65
Q

T/F. Second-impact syndrome is often lethal, but is rare.

A

True

66
Q

What does Second-impact syndrome cause? And what can that lead to?

A

Involves rapid brain swelling, increased ICP, cerebral herniation —> which causes disability, coma, or death

67
Q

Brain bleeds aren’t always ass. with concussions, but when they are what is indicative of it?

A

Progressively worsening neurological abnormalities

–medical emergency!!!

68
Q

What are some examples of Progressively worsening neurological abnormalities?

A
  • repeated vomiting
  • worsening HA
  • sustained or worsening vision
  • dysphagia
  • ataxia
69
Q

How would one rule out a intracranial hemorrhage that could occur with a concussion?

A

CT scan

70
Q

What forms of intracranial hemorrhage are more likely to occur following a trauma?

A
  1. Epidural hematoma

2. Subdural hematoma

71
Q

What develops following the traumatic disruption of dural ARTERIES?

A

Epidural hematoma

72
Q

What is the MC disrupted artery of an Epidural hematoma?

A

middle meningeal artery

73
Q

How do Epidural hematomas manifest? How lethal are they?

A

due to it being an artery–> accumulate very rapidly

could be lethal within hours (medical emergency!)

74
Q

T/F. Epidural hematomas are MC than subdural hematomas, and are ass. with a skull fracture.

A

False– epidural hematomas are LESS common (2%) than subdural hematomes; but YES, epidural hematomas do commonly cause skull fx

75
Q

What develops following the traumatic disruption of the bridging subdural veins extending from cerebral hemispheres to the dural sinuses?

A

Subdural hematomas (involves veins)

76
Q

How do Subdural hematomas manifest? How lethal are they?

A

slowly manifest (due to veins involved) and may clot and self-resolve w/o Tx

if large enough may be lethal w/in couple

77
Q

T/F. Since subdural hematomas involve a vein, they are not a medical emergency

A

False– an immediate neurosurfical referral is necessary

78
Q

What percentage of severe head injuries are subdural hematomas suspected to develop in?

A

25%–> therefore MC than epidural hematomas

79
Q

Are Subdural or Epidural hematomas most likely to affect infants and geriatics?

A

subdural hematomas are

80
Q

If an infant develops a subdural hematoma, what is most likely the cause?

What are if a geriatric ind. develops one?

A

infant–> MC victim of child abuse

Geriatric –> following cerebral atrophy making subdural veins taught and vulnerable to disruption–> and minor fall or trip could cause minor amount of head trauma and cause this

System Pathology I -- Roecker (14 decks)

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