Ch 2 - TBI: Pathophysiology Flashcards

1
Q

What is the MCC of head injury in adolescents and adults?

A

Motor vehicle accidents (~50% of cases)

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2
Q

What is the single MCC of death and injury in automobile accidents?

A

Ejection of occupant from the vehicle

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3
Q

What is the married status of patients with TBI?

A

Single (47%) > married (32%) > divorced (16%) > widowed/separated (5%)

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4
Q

What % of TBI etiology involve alcohol?

A

> 50%

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5
Q

What is Primary Injury in TBI?

A

Direct disruption of brain parenchyma from shear forces of the impact occurring immediately and not amenable to medical intervention

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6
Q

What are types of Primary Injury in TBI?

A

Contusion
Diffuse axonal injury (DAI)
Impact depolarization

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7
Q

What is brain contusion?

A

Bruising of the cortical tissue

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8
Q

What is Diffuse axonal injury (DAI)?

A

Immediate disruption of the axons due to acceleration–deceleration and rotational forces that cause shearing upon impact

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9
Q

What is secondary axotomy in DAI due to?

A

Increased axolemma permeability, calcium influx, and cytoskeletal ABN that propagate after the injury

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10
Q

What is the characteristic of DAI on imaging?

A

White matter petechial hemorrhages

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11
Q

What is impact depolarization?

A

Massive surge in extracellular K+ and glutamate release (excitatory) occurs after severe head injury and leads to excitotoxicity (secondary injury)

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12
Q

What are types of secondary injury in TBI?

A

Ischemia, excitotoxicity, energy failure, and resultant apoptosis
Brain swelling/edema
Axonal injury
Inflammation and regeneration

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13
Q

What is excitoxicity?

A

NT (glutamate) causes calcium influx, oxygen-free radical release, lipid peroxidation, mitochondrial failure, and DNA damage > nerve cell death

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14
Q

When does brain swelling occur after TBI?

A

w/in 24 hours due to an increase in cerebral blood volume (intravascular blood).

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15
Q

How is brain swelling identified on CT?

A

Collapse of ventricular system and loss of CSF cisterns around the midbrain

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16
Q

When does brain edema occur after TBI?

A

Later than brain swelling due to an inc in brain volume 2/2 inc brain water content > extravascular fluid

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17
Q

What is the pathophysiology of vasogenic brain edema?

A

Outpouring of protein rich fluid through damaged vessels

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18
Q

What pathology is vasogenic brain edema related to?

A

Extracellular edema

Cerebral contusion

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19
Q

What is the pathophysiology of cryptogenic brain edema?

A

Failing of the cells’ energy supply system > inc cell-wall pumping system> intracellular edema in the dying cells

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20
Q

What pathology is cryptogenic brain edema related to?

A

Hypoxic and ischemic brain damage

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21
Q

What is focal injury in TBI?

A

Localized injury in the brain occurring immediately after the injury and easily visualized by CT or MRI

22
Q

What are types of focal injury in TBI?

A

Cerebral contusions
Focal ischemia
Focal hemorrhages

23
Q

How do cerebral contusions occur?

A

Brain hits the inner table of the skull

24
Q

Where do cerebral contusions typically occur?

A

Inferior frontal lobe and anterior portion of the temporal lobe

25
How does focal ischemia occur (pathophysiology)?
2/2 vasospasms after a traumatic SAH or from physical compression of the arteries
26
What are types of focal hemorrhages?
Epidural Subdural Subarchnoid
27
How do epidural hemorrhages occur?
90% temporal bone fx over the middle meningeal artery or veins
28
What is the clinical presentation of epidural hemorrhages?
Lucid interval (50%) prior to rapid deterioration
29
What is seen on CT in epidural hemorrhages?
Biconvex acute hemorrhagic mass
30
What limits hematoma expansion in epidural hemorrhages?
Tight adherence of the dura to the skull
31
How do subdural hematomas occur?
Shearing of the bridging veins between the pia-arachnoid and the dura
32
Why are subdural hematomas typically larger in elderly patients?
Due to generalized loss of brain parenchyma
33
What is seen on CT in subdural hematomas?
High density, crescentic, extracerebral masses
34
When is the presentation of symptoms in subdural hematomas?
Acute SDH: Immediate sx Subacute SDH: 3 days-3 wks Chronic SDH: > 3 weeks
35
How do subarchnoid hemorrhages occur?
Ruptured cerebral aneurysms and AVMs Leakage from an intraparenchymal hemorrhage Trauma
36
What is seen on CT in subarchnoid hemorrhages?
Blood w/in the cisterns and subarachnoid space ~ 24 hr
37
When does CT sensitivity decrease in subarchnoid hemorrhages?
Dec to 30% 2 weeks after the initial bleed
38
What is a grade I DAI?
Widespread white matter/axonal damage but no focal abnormalities on imaging
39
What is a grade II DAI?
Widespread white matter/axonal damage, and focal findings (MC in the corpus callosum)
40
What is a grade III DAI?
Damage involving the brainstem
41
When is DAI initiated?
Time of the injury by axonal shearing from acceleration–deceleration rotational forces
42
What is the MCC of unconsciousness during first 24 hours after DAI?
Axonal injury
43
Which types of TBI have a higher risk of posttraumtic epilepsy?
Penetrating head injuries
44
What is brain plasticity?
Capability of the damaged brain to “repair” itself by means of morphologic and physiologic responses
45
What is brain plasticity influenced by?
Environment Complexity of stimulation Repetition of tasks Motivation
46
What are the two mechanisms of brain plasticity?
- Neuronal regeneration/neuronal (collateral) sprouting | - Functional reorganization/unmasking neural reorganization
47
What is Diaschisis?
Damage to one region of the CNS alter function of uninjured area fiber tracts causing loss of function at both sites
48
How does functional/behavioral substitution help recovery in TBI?
New strategies are learned to compensate for deficits and to achieve a particular task
49
How does redundancy help recovery in TBI?
Uninjured brain areas normally contribute same function of injured brain
50
How does vicariation help recovery in TBI?
Brain areas alter their properties in order to subserve that function