Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

529 Neuro 2 > L2 Mod/Severe TBI > Flashcards

L2 Mod/Severe TBI Flashcards

(73 cards)

Start Studying
1
Q

types of mod/severe brain injuries

A

acquired brain injury
stroke
blunt trauma
coup-contra coup injury
shaken baby syndrome
diffuse axonal injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

anoxic brain injury

A

occlusion of oxygen
15 s can cause loss of consciousness
4 minutes severe injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

hypoxic brain injury

A

caused by not enough O2 saturation in air like at altitude
suffocation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

causes of TBI

A

falls
blunt trauma
car accident
assault

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

incidence of TBI - population

A

highest in teenagers/20s and after 75 due to falls

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

immediate damage after brain trauma

A

scalp laceration
fracture
cerebral contusion
cerebral laceration
intercranial hemorrhage
diffuse axonal injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

delayed secondary damage after brain trauma

A

ischemia
hypoxia
cerebral swelling
infection
events evolving over time
+ elevated ICP and edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

diffuse axonal injury - primary damage

A

axons are sheared by deceleration/acceleration/rotational injuries
axons twist and tear leading to neuronal death
white matter injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

grades of DAI

A

1: mild, microscopic changes in midbrain
2: local lesions, corpus callosum
3: severe focal lesions on brainstem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

recovery after DAI

prognosis, % of people recovering

A

50% of people have good recovery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

dural hematoma - primary damage

A

skull fracture can tear menigeal arteries/vessels/sagittal sinus
causes bleed until the dura or above

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

penetrating brain injuries - primary damage

A

can survive puncture in cerebrum with memory and cognition changes
brain stem injury mostly fatal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

cellular complications with TBI

A

inflammation/ROS generation
excitotoxicity
BBB damage
mitochondrial dysfunction
damage causes glutamate increase and excitotoxicity with reactive oxygen species, neutrophils and microglia cross BBB, cerebral edema, death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

microglia activity after injury

A

increasing up to 30 days after injury, specifically the neurotoxic type

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

primary types of injury in TBI

A
  1. DAI (3 grades of severity)
  2. Dural hematoma
  3. penetrating injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Secondary damage after TBI includes:

A

cerebral edema/vasospasm/ICP increase
increased glutamate release
excitotoxicity
inflammation and ROS generation
impaired GLC metabolism
BBB damage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

cascade of secondary damage after TBI (order of events)

A

TBI causes:
1. exocytosis
2. structural damage
3. BBB damage and glutamate affected permeabiliity
4. glutamate transporter impairment
Then:
glutamate levels increase due to brain trauma
Then:
glutamate receptors are excessively activated
leading to: excitotoxicity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

How does excitotoxicity affect the brain physiologically?

A

increases Ca entry into cells
cerebral edema
cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

how is BBB affected by TBI?

A

inflammatory markers, ROS, glutamate lead to larger gaps in the BBB
these allow neutrophils and activated microglia to enter
increasing risk of infection and inflammation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

microglia activity after TBI

A

immediate: protective microglia levels increase over 1-2 days then decrease; low level of toxic microglia
10-12 days post injury: toxic microglia increase for up to a month as protective microglia have decreased levels
microglia levels determine degree of secondary injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

TBI contributes to what condition later in life?

A

dementia, Alzheimer’s, chronic neurocognitive impairment

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

mTBI mechanism contributing to dementia

A

repetitive mTBI
creates edema
axonal alterations/protein aggregates
neurofibrillary tangles form + genetic influence
dementia onset or Alzheimer’s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

severe TBI mechanism contributing to Alzheimer’s

A

impaired neuronal homeostasis over long term leads to protein aggregates
Amyloid beta plaques form
Alzheimer’s develops

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

prefrontal cortex control:

A

working memory
self control/irritability
decision making

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
amygdala controls:
emotional regulation fear response
26
hippocampus controls:
learning memory
27
motor impairments can come from damage in these areas of the brain:
brainstem mid brain cerebellum cortex BG
28
neurocognitive impairments in brain injury include:
memory: STM, LTM, procedural judgment language/aphasia sleep/wake cycle, arousal
29
behavioral impairments in brain injury include:
impulsivity irrational out of context behaviors personality changes
30
motor impairments from brain injury include:
hemiparesis ataxia synergistic movement hypertonia - spasticity, contractures tremors - impairments depend on damaged area(s)
31
reticular activating system control:
waking: thalamic input increases to increase arousal; pt increases attention and appropriate responses to stimuli sleeping: reduction in sensory info and atonia to not activate movement fight or flight: ANS function with hypothalamus and circadian rhythm
32
reticular formation functions
integration, relay, coordination center for life functions including: circadian rhythm, sleep/wake cycle, coordinate somatic motot movements, CV/resp control, pain modulation, habituation to sensation CN motor nuclei for respiration
33
CN involved in respiration
trigeminal, facial, glossopharyngeal, vagus, hypoglossal
34
mechanism of sleep dysfunction after TBI
frontal temporal lobe primary and secondary damage results in reduced melatonin hypothalamus damage: suprachiasmistic nucleus assists circadian rhythm by making melatonin long pathway damage interrupts melatonin production
35
type of memory disruption common in mild/mod TBI
STM, learning
36
type of memory disruption common in severe TBI
LTM due to hippocampus and cortex damage will need to relearn procedural memory like walking, bed mobility, etc
37
mechanism of memory loss in TBI
hippocampus and cortex/pre-frontal cortex interact w hippocampus retrieving, storing, and recalling spatial info and identification info + procedural memory damage to any of these areas can disrupt this process
38
how to improve memory in therapy for mod/severe TBI
incorporate memory into therapy exercises ex) ask pt to recall where they put an object work on compensatory strategies like memory book
39
What neurochemicals increase w exercise to benefit healing in TBI?
BDNF, orexin A + neuroprotective microglia + antiinflammatory cytokines
40
effect of BDNF on brain
increased long term potentiation, plasticity, and neurogenesis in the hippocampus leads to cognitive improvements, mood improvements, and prevention of neurodegeneration helps repair after damage from TBI
41
effect of Orexin A on brain
increased long term potentiation, plasticity, and neurogenesis in the hippocampus leads to cognitive improvements, mood improvements, and prevention of neurodegeneration
42
What neurochemicals decrease w exercise to benefit healing in TBI?
proinflammatory cytokines neurotoxic microglia
43
extent of secondary injury timeline after TBI
days - months - years depending on pt, condition, social support, rehab
44
medical sequelae after TBI
increased ICP caused by: edema, hemorrhage, hematoma must be monitored for acute hydrocephalus
45
red flag s/s of acute hydrocephalus
pupillary changes headache vomiting
46
mobilization with EVD
early mobilization improves outcomes after a craniotomy and extraventricular drain
47
a ventricular catheter monitors what?
ICP
48
brain bolt monitors
brain oxygenation
49
indications for decompressive craniectomy
massive ICP not relieved by burr hole
50
How to mobilize patient with EVD
must be clamped by nursing before mobilizing at all, including changing HOB height or bed mobility monitor cerebral perfusion pressure, ICP, HR, BP, O2
51
basic ways ICP is monitored and lowered
monitored to be <20 mmHg if high: 1. 30 degree HOB elevation, sedation, O2 sats 92%, decrease CO2, CSF drain 2. hyperventilation, mannitol, barbituates 3. hyperosmolar solution, hyperventilation, decompressive craniectomy, hypothermia
52
loss of consciousness defitinion
several minutes to hours/days
53
coma definition
complete paralysis of cerebral function unresponsive state GCS: eyes closed, no response to pain, sound, tactile stim
54
persistent vegetative state
reduced responsiveness with no evidence of cortical function due to diffuse hypoxia, axonal white matter damage
55
mTBI GCS scores
13-15
56
mod TBI GCS scores
9-12
57
severe TBI GCS scores
<9
58
post traumatic amnesia, mTBI
<1 day
59
post traumatic amnesia, mod TBI
1-7 days
60
post traumatic amnesia, severe TBI
>7 days
61
LOC time, mTBI
0-30 min
62
LOC time, mod TBI
30 min-24 hours
63
LOC time, severe TBI
>24 hours
64
GCS: eye opening scores
1-4 4 - spontaneous 3 - to voice 2 - to pain 1 - no repsonse
65
GCS: verbal response
1-5 5: normal conversation 4: disoriented conversation 3: words, not coherent 2: sounds only 1: no response
66
GCS: motor response
1-6 6: normal 5: localized to pain 4: withdraws to pain 3: decorticate posture/flexor synergy 2: decerebrate posture/extensor synergy 1: no response
67
subgroups of severe brain injury
includes prolonged state of unconsciousness for days-months -coma -vegetative state - persistent vegetative state - minimally responsive state - locked in syndrome
68
rancho los amigos levels of cognitive functioning (simplified)
1: no response 2: generalized response, inconsistent, not in response to stim 3: localized response to stim 4. agitated and confused 5. inappropriate, non agitated, confused 6. confused appropriate response to commands 7. automatic appropriate, person has minimal confusion 8. functioning memory, response to environment, unaware of some deficits 9. does daily routine, aware of need for assistance 10. normal function/modified independent, does daily routine with or without compensation
69
possible motor issues in TBI
weakness contractures spasticity/hypertonia coordination from cerebellum or BG balance synergistic postural misalignment motor planning (prefrontal cortex)
70
cognitive assessment in mod/severe TBI should include:
arousability: what stim arouses pt alertness orientation: self, place, time following directions: # of steps memory: spatial, idetify, procedure judgement: transfers/gait
71
agitated behavior scale (ABS)
assesses pts in the acute phase for issues such as: violence, anger pulling at tubes, mood changes, impulsivity each behavior scored 1-4 from absent to present to extreme level
72
functional assessment of mod/severe TBI should include:
bed mobility transfers upright stability gait
73
what environmental factors could affect TBI treatment?
light background noise people in room extra movement

529 Neuro 2 (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions