Exam 4: Chapters 36 and 6 Flashcards

1
Q

What 3 elements must be balanced to maintain ICP?

A

brain tissue, csf, and blood

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2
Q

What is a normal ICP?

A

7-15mmHg

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3
Q

What can cause an increase to ICP?

A

trauma, edema, increased csf, hemorrhage, tumor, inflammation, ischemia, blockage of venus return, vasodilation

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4
Q

What are early signs of increased ICP?

A

vomiting, severe headache, decreased LOC (confusion and drowsy)

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5
Q

What are the late sx of increased ICP?

A

Cushing triad (systolic HTN, bradycardia, bradypnea), worsening LOC, posturing (decorticate or decerebrate), altered pupil size and response to light

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6
Q

What is the Glasgow Coma Scale?

A

measures a pts consciousness by eye opening response, verbal response, and motor response

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7
Q

What is brainstem herniation?

A

when to much downward pressure is put on the brain due to increased ICP that leads to death

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8
Q

What are caused of TBI?

A

coup-contrecoup, penetrating injury, blunt injury, and blast injury

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9
Q

Causes of Diffuse Axonal Injury

A

coup-contrecoup

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10
Q

Risk factors for Diffuse Axonal Injury

A

motor vehicle accident, fall, sports, violence/abuse

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11
Q

Pathophysiology of Diffuse Axonal Injury

A

shearing/ tearing of an axon that leads to bleeding, swelling, brain cell damage, and impairment of signal transmission. there is decreased blood flow to the brain

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12
Q

Sx of Diffuse Axonal Injury

A

loss of consciousness and pt may never regain consciousness. if pt does then significant neurological impairment is possible

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13
Q

Cause of a concussion

A

blunt trauma and coup-contrecoup

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14
Q

Risk factors of a concussion

A

motor vehicle accident, contact sports, violence/abuse

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15
Q

Pathophysiology of a concussion

A

mild TBI that causes a temporary neuronal cellular swelling that resolves over time

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16
Q

Sx of a concussion

A

headache, brief loss of consciousness, nausea, flat affect, lack of coordination, brief amnesia, “seeing stars”

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17
Q

Causes of a cerebral contusion

A

coup-contrecoup, blunt trauma, penetrating injury

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18
Q

Risk factors of cerebral contusion

A

anticoagulants, contact sports, fall

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19
Q

Pathophysiology of cerebral contusion

A

vascular and tissue damage; cerebral edema is present 48-72 hours after injury

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20
Q

Sx of a cerebral contusion

A

severe headache, dizziness, vomiting, increased size of pupil (ipsilateral), sudden weakness in arm or leg (contralateral), restless, agitated, irritable, memory loss

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21
Q

Causes of intracranial bleed

A

coup-contrecoup, blunt trauma, penetrating injury

22
Q

Causes of an epidural hematoma

A

skull fracture lacerating the cerebral and meningeal artery

23
Q

Sx of a EDH

A

headache, midline shift, hemiplegia contralateral to injury, sx of increased ICP, seizures, rapid worsening status, and late sx include crushing’s triad

24
Q

Causes of a subdural hematoma

A

tearing of veins in subdural space, csf may leak into subdural space; characterized by slow bleeding that can take days to accumulate

25
Sx of a SDH
may or may not cause a midline shift
26
Causes of a subarachnoid hemorrhage
tearing of the cerebral and meningeal vessels or rupture of a cerebral artery that fills the subarachnoid space
27
Sx of a SAH
worst headache of pts life, diplopia, nuchal rigidity, stroke sx, often unconscious
28
Causes of a skull fracture
blunt trauma
29
Sx of a skull fracture
battle sign, racoon eyes, csf otorrhea, csf rhinorrhea
30
What is a primary spinal cord injury?
injury caused by trauma
31
What is a secondary spinal cord injury
injury caused by ischemia that is worsened by damage from primary injury
32
What deficits are caused by descending injury
motor
32
What deficits are caused by ascending injury?
sensory
32
What is caused by a complete transection
motor and sensory deficits that is a permanent injury
33
What is an incomplete injury (transection)?
injury where some function may return
34
What are the mechanisms of injury in SCI?
hyperflexion, hyperextension, rotation, vertical compression, penetrating injury
35
What is spinal shock?
shock that is not about perfusion; long term function is unknown until after spinal shock resolves
36
Sx of spinal shock
loss of bowel and bladder control, loss of (motor movement, sensation, vasoconstriction, shivering) at and below level of injury, if cervical it may impact breathing
37
What is neurogenic shock?
shock that is influenced by perfusion, only if injury is at T6 or above and affects the SNS
38
Sx of neurogenic shock
decreased cardiac output, hypotension, inadequate perfusion, bradycardia, vasodilation
39
What are the systemic complications of SCI?
cardiovascular (orthostatic HTN), autonomic dysreflexia, cervical and thoracic injuries weaken breathing and increase the risk of respiratory infection, weaken the immune system, neuropathic pain
40
What is the gate control theory?
when pain is occurring at two or more sites the pt will only report one
41
What is the neuromatrix theory
emphasizes that the brain has an influence in pain experiences
42
What is an open gate?
interneuron allows transmission of pain stimulus from the periphery to ascend the spinal cord to the brain
43
What is a closed gate?
interneuron does not allow transmission of neural stimulus from pain fibers in the periphery
44
How can pain occur?
noxious stimulation of nociceptors or no obvious stimulation to nociceptors
45
What are the different types of pain?
acute, chronic, neuropathic
46
What are the different sources of pain?
cutaneous, deep somatic, visceral pain
47
Which neurotransmitters enhance pain?
prostaglandins, interleukins, tumor nectroic factor, leukotrienes, bradykinins
48
Which neurotransmitters amplify pain?
substance p and glutamate
49
Which neurotransmitters inhibit pain?
endorphins, enkephalins, acetylcholine, dopamine, gamma-aminobutyric acid, norepinephrine, serotonin