Patho 2 Flashcards

1
Q

What direction is bad in skull fractures

A

in is bad

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2
Q

what are risks associated with depressed skull fractures

A
  • disruption of tightly adherent dura
  • tear of meningeal vessels
  • contuse/lacerate underlying brain tissue
  • can communicate with facial sinuses (MC maxillary) or middle ear
  • infection/meningitis
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3
Q

Thinnest part of the skull is where? what blood vessel is associated?

A
  • near the temple

- middle meningeal artery (epidural)

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4
Q

What are the sx of a basal skull fracture?

A
  • raccoon eyes

- CSF leak out nose or ear

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5
Q

What is best imaging for skull fracture?

A

CT!!! Don’t bother with plain film

- start w/o, once r/o bleed, then can do contrast if needed

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6
Q

What is common secondary issue with brain injury?

A

Coup contracoup injury

  • coup at site of injury
  • contracoup opposite side of injury
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7
Q

Concussion

A
  • occurs after trauma in absence of demonstrable damage to cranium or brain
  • transient loss of consciousness
  • amnesia (retro- and anterograde)
  • minor damage to CNS
  • lasting effects are minimal unless injury is repetitive
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8
Q

Dementia pugilistica

A

“punch drunk”

- fighters in past who had damage due to multiple concussions

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9
Q

Brain contusion
- caused by waht
- level of damage
-

A
  • d/t violent motion or fast stopping - brain hits calvarium (skull)
  • shaken baby syndrome and acceleration/deceleration injuries
  • produces underlying local damage
  • can be transient/minor OR produce enough damage to cause epilepsy
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10
Q

Brain contusion

- common brain locations of damage

A
  • inferior surface of frontal lobes
  • anterior tip of temporal lobes
  • occipital poles
    • may act as foci of seizure activity, esp. temporal lobes
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11
Q

Where is location of middle meningeal artery bleed?

A

Epidural

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12
Q

What type vasculature is typically bleeding in subdural bleeds?

A
  • Venous – cerebral veins

- Lower pressure, sx over a longer period of time compared to epidural bleed

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13
Q

What type of bleeds will produce blood in a spinal tap?

A
  • Subarachnoid – blood is between arachnoid and pia where CSF is
  • Not subdural
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14
Q

Epidural hematoma

  • location
  • cause
  • sx
  • tx
A
  • Between skull and dura mater
  • Tearing of middle meningeal artery
  • Characterized by transiet loss of consciousness with subsequent lucid interval
  • 2 hours to repair!
  • Surgical drainage prevents rapid expansion, brain herniation, death
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15
Q

Subdural hematoma associated with what cause

A

blunt trauma w/o overlying skull fx

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16
Q

Subdural hematoma acute vs. chronic

A

Acute

  • Become clinically apparent a few days after trauma
  • Fluctuating levels of consciousness

Chronic

  • Clinically apparent weeks or months after trauma
  • Slowly developing confusion/inattention, eventually coma
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17
Q

Symptoms of ICP

A
  • HA
  • vomiting
  • drowsy
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18
Q

Describe a subarachnoid hemorrhage

A
  • damage to blood vessels on surface of the brain (in the pia)
  • Trauma most common, can also be aneurysm or arteriovenous malformation
  • Does result in bloody tap
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19
Q

What causes papilledema

A
  • Increased CSF, commonly subarachnoid hemorrhage

- Epidural and subdural less likely but possible if large enough

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20
Q

What should never be done if suspect increased ICP?

A

Spinal tap, risk for herniation in brain (very bad)

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21
Q

What areas of brain are most sensitive to hypoxia?

A

Medial temporal lobe (contains hippocampus)

22
Q

What do neurologic changes due to hypoxia depend on?

A

Extent and duration of the hypoxia

- severe deficits can be cleared completely if hypoxia is revered quickly

23
Q

How long might sx dt hypoxia take to resolve?

A

One year, after that unlikely to see additional improvement

- it is the secondary area that is recovering (the part that was damaged by glutamate release)

24
Q

Is acute hypoxia or chronic hypoxia worse?

A

Acute is more damaging

25
Q

What are the four types of stroke?

A
  1. Ischemic d/t thrombosis
  2. Ischemic d/t emboli
  3. Intracerebral hemorrhagic
  4. Extracerebral hemorrhagic
26
Q

Is ischemic or hemorrhagic stroke more likely?

A

Ischemic – people live longer with more atherosclerosis

27
Q

Ischemic stroke

  • how fast is death
  • Main cause
A
  • Death rarely in first hour, more likely to survive than hemorrhage
  • Atherosclerosis
28
Q

Hemorrhagic stroke

  • How fast is death
  • Main cause for intracerebral and extracerebral
A
  • Death more likely in first hour (than in ischemic)
  • Intracerebral: striate arteries rupture (d/t HTN)
  • Extracerebral: arteriovenous malformation or aneurysm
29
Q

Stroke risk factors

A
  • HTN
  • smoking
  • DM
  • HIV tx (elevates cholesterol)
  • bruits
  • previous TIAs
  • Protein C or S deficiency
  • Factor V Leiden
  • OCP
  • fam hx
  • age
  • a-fib
  • AA
30
Q

With what sx do you workup for stroke?

A
  • HA!
  • LOC – only if large bleed
  • focal deficits initially unlikely
31
Q

Sx of intracerebral bleed

A
  • HA only if large
  • LOC possible (usually dt uncontrolled HTN)
  • always local deficits bc of location
32
Q

Sx of Ischemic stroke

A
  • HA unlikely
  • LOC unlikely
  • Large focal deficits dt death of downstream neurons
33
Q

Cincinnati stroke sx

A
  1. Facial droop
  2. arm drift
  3. slurred speech

1 sx = 70% likely having stroke
2+ sx = 90%+ having stroke

34
Q

Infarction

- cause

A
  • vascular thrombosis

- related to pre-existing damage to vessel wall such as atherosclerosis

35
Q

Infarction

  • common location
  • common population
  • usually preceded by what?
A
  • Common within larger vessels (internal carotid, vertebral, basilar)
  • Mostly in older pts
  • Commonly preceded by TIAs
36
Q

What is a TIA

A

Acute onset of neurologic sx that resolve in minutes to hours

37
Q

Amaurosis fugax

A

TIA of visual field

38
Q

Emboli cause of infarction

  • Describe
  • Sx
A
  • emboli break off thrombi in left heart or carotid
  • Tend to be multiple and involve smaller vessels
  • sudden onset of neurological deficit
39
Q

What do infarction sx depend on?

A

Location and size of infarct

40
Q

Infarction sx

A
  • Can be as mild as confusion or a change in bp

- Hard to distinguish from hemorrhage based on presentation or early imaging

41
Q

How treat infarction?

A
  • TPA w/in 3 hours of focal neurologic sign (and have ruled out hemorrhage)
42
Q

What is significant about the 3 hour mark for TPA

A
  • cut off for risk of bleed vs. likelihood for improvement.
  • might be more willing to give TPA to young person later than 3 hours
  • old person wakes up with focal symptoms, not going to give them TPA bc don’t know how long sx started and risk for bleed isn’t worth it
43
Q

Non-traumatic hemorrhagic stroke

  • describe
  • commonly associated with what
A
  • not located in a specific part of brain, will expand, doesn’t obey borders
  • unlike infarcts, not limited to arterial distribution
  • HTN
44
Q

Non-traumatic hemorrhagic stroke

- type of damage in brain

A
  • compress and disrupt parenchyma vs. destroy it
  • may rupture into ventricular system
  • herniation may occur secondary to expanding mass
45
Q

Berry aneurysms

  • aka
  • how common?
  • where occur?
A
  • saccular aneurysms
  • 5-6% of population (eeek)
  • middle cerebral artery and it’s branches (more often anterior, communicating, and internal carotid than posterior circulation)
46
Q

Berry aneurysm

- presentation

A
  • usually as spontaneous rupture
  • display sx of stroke
  • may lead to sudden death
47
Q

Berry aneurysm tx

A
  • if has a stalk - clip it

- no stalk - coil

48
Q

Vascular malformations

  • how common
  • two types
A
  • 5% of population
  • venous (more common)
  • arteriovenous
49
Q

Venous malformations

- sx

A

usually asymptomatic

50
Q

Arteriovenous malformations

- risk compared to venous

A
  • more likely to rupture