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Pathophysiology > Exam 4: Chapters 36 and 6 > Flashcards

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
Q

Sx of a SDH

A

may or may not cause a midline shift

26
Q

Causes of a subarachnoid hemorrhage

A

tearing of the cerebral and meningeal vessels or rupture of a cerebral artery that fills the subarachnoid space

27
Q

Sx of a SAH

A

worst headache of pts life, diplopia, nuchal rigidity, stroke sx, often unconscious

28
Q

Causes of a skull fracture

A

blunt trauma

29
Q

Sx of a skull fracture

A

battle sign, racoon eyes, csf otorrhea, csf rhinorrhea

30
Q

What is a primary spinal cord injury?

A

injury caused by trauma

31
Q

What is a secondary spinal cord injury

A

injury caused by ischemia that is worsened by damage from primary injury

32
Q

What deficits are caused by descending injury

A

motor

32
Q

What deficits are caused by ascending injury?

A

sensory

32
Q

What is caused by a complete transection

A

motor and sensory deficits that is a permanent injury

33
Q

What is an incomplete injury (transection)?

A

injury where some function may return

34
Q

What are the mechanisms of injury in SCI?

A

hyperflexion, hyperextension, rotation, vertical compression, penetrating injury

35
Q

What is spinal shock?

A

shock that is not about perfusion; long term function is unknown until after spinal shock resolves

36
Q

Sx of spinal shock

A

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
Q

What is neurogenic shock?

A

shock that is influenced by perfusion, only if injury is at T6 or above and affects the SNS

38
Q

Sx of neurogenic shock

A

decreased cardiac output, hypotension, inadequate perfusion, bradycardia, vasodilation

39
Q

What are the systemic complications of SCI?

A

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
Q

What is the gate control theory?

A

when pain is occurring at two or more sites the pt will only report one

41
Q

What is the neuromatrix theory

A

emphasizes that the brain has an influence in pain experiences

42
Q

What is an open gate?

A

interneuron allows transmission of pain stimulus from the periphery to ascend the spinal cord to the brain

43
Q

What is a closed gate?

A

interneuron does not allow transmission of neural stimulus from pain fibers in the periphery

44
Q

How can pain occur?

A

noxious stimulation of nociceptors or no obvious stimulation to nociceptors

45
Q

What are the different types of pain?

A

acute, chronic, neuropathic

46
Q

What are the different sources of pain?

A

cutaneous, deep somatic, visceral pain

47
Q

Which neurotransmitters enhance pain?

A

prostaglandins, interleukins, tumor nectroic factor, leukotrienes, bradykinins

48
Q

Which neurotransmitters amplify pain?

A

substance p and glutamate

49
Q

Which neurotransmitters inhibit pain?

A

endorphins, enkephalins, acetylcholine, dopamine, gamma-aminobutyric acid, norepinephrine, serotonin

Pathophysiology (8 decks)

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