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Pathophysiology > Chapter 17- Central & Peripheral Nervous Systems > Flashcards

Chapter 17- Central & Peripheral Nervous Systems Flashcards

1
Q

primary spinal cord injury

A

occurs w/ initial mechanical trauma & immediate tissue destruction. Occurs if spine not adequately immobilized following injury.

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2
Q

secondary spinal cord injury

A

complex phathophys. cascades of vascular, cellular & biochemical events that begin within a few mins after injury & cont. xweeks

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3
Q

Ex secondary spinal cord injuries

A

hemorrhages, inflammation, edema, ischemia

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4
Q

What’s the concern in C1-C4 cervical spinal cord injury?

A

swelling may be life-threatening b/c cardiovascular and respiratory control functions could be lost

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5
Q

Pathophys. behind cardiovascular and respiratory control function loss in cervical cord injuries

A

Similar to TBI, excitotoxicity (stim of excitatory neurotransmitters like glutamate), intracellular Ca overload, oxidative damage, & cell death

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6
Q

patho vertebral injuries

A

acceleration, deceleration, or deformation forces occurring at impact causing vertebral fx, dislocation, & penetration of bone fragments that can cause compression to tissue, pull/exert traction on tissue, or cause shearing of tissues so they slide into one another

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7
Q

Most common areas for vertebral injuries in adults

A

C1-C2, C4-C7, T10-L2 (most mobile portions)

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8
Q

Spinal shock

A

temporary loss of spinal cord functions below lesion immediately after injury

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9
Q

causes of spinal shock

A

cord hemorrhage, edema, or anatomic transection

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10
Q

clinical manifestations spinal shock

A

Spinal cord activity below injury ceases
1. complete loss of reflex function
2. flaccid paralysis
3. absence of sensation
4. loss of bladder/rectal control
5. transient drop in BP
6. bradycardia
7. poor venous circulation
8. disturbed thermal control
9. respiratory impairment

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11
Q

Termination/resolution of spinal shock

A

Lasts 2-3 days. Terminates with reappearance of:
1. reflex activity
2. hyperreflexia
3. spasticity
4. reflex emptying of bladder

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12
Q

What is Neurogenic/Vasogenic shock

A

Absence of sympathetic activity through loss of supraspinal control and unopposed parasympathetic tone mediated by the intact vagus nerve

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13
Q

Who is at risk for neurogenic shock

A

cervical or upper thoracic cord injuries above T6 maybe in addition to spinal shock.

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14
Q

S/S neurogenic shock

A
  1. vasodilation
  2. hypotension
  3. bradycardia
  4. failure of body temp regulation
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15
Q

Quadriplegia & what injury causes

A

paralysis (complete or incomplete/partial loss of upper extremity function) in all 4 extremities; level of injury is above C6

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16
Q

what’ s autonomic hyperreflexia (dysreflexia)

A

syndrome of sudden massive reflex sympathetic discharge associated with spinal cord injury at level T6 or above

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17
Q

S/S autonomic hyperreflexia/dysreflexia

A
  1. paroxysmal HTN (up to 300 mm HG SBP)
  2. pounding HA
  3. blurred vision
  4. sweating above level of lesion w/ flushing of skin
    5 nasal congestion
  5. nausea
  6. piloerection (pilomotor spasm)
  7. bradycardia (30-40 bpm)
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18
Q

What can dysreflexia lead to if untreated

A

stroke, seizure, MI, death
requires immediate tx

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19
Q

Patho dysreflexia

A

sensory receptors below level of cord lesion stimulated > autonomic NS increases BP > baroreceptors stim. parasympathetic decreasing HR but visceral & peripheral vessels don’t dilate bc impulses can’t pass through cord

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20
Q

Most common cause dysreflexia

A

1 distended bladder or rectum

any sensory stim. can cause

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21
Q

What’s herniated disc

A

displacement of nucleus pulposus or annulus fibrosus beyond intervertebral disk space

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22
Q

Risk factors herniated disc

A
  1. weight-bearing sports
  2. light weight lifting
  3. certain work activities like repeated lifting
  4. Men > women
  5. 30-50 y/o
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23
Q

Where does disc herniation usually occur

A

LOW
L4-L5, L5-S1
Sometimes cervical C5-C6, C6-C7. Thoracic rare

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24
Q

Radiculopathy

A

R/t disc herniation
“pinched nerve”; injury or damage to nerve roots in the area where they leave the spine
Dermatomal distribution from compression, inflammation, or both of spinal nerve from herniated disc

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25
Q

Clinical manifestation herniated dic lumbarsacral region

A
  1. pain radiates along sciatic nerve over buttock into calf or ankle that occurs with straining (coughing, sneezing) & straight leg rise
  2. limited ROM lumbar spine
  3. tenderness on palp. sciatic notch & along sciatic nerve
  4. impaired pain, temp, touch sensations leg/foot
  5. decreased/absent ankle jerk reflex
  6. mild weakness of foot
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26
Q

Clinical manifestation herniated dic lower cervical region

A
  1. paresthesias & pain upper arm/forearm/hand along nerve root
  2. neck motion & straining increase pain
  3. neck ROM diminished
  4. weakness/atrophy biceps/triceps
  5. decreased reflex biceps/triceps
  6. may have motor/sensory weakness/disturbance BLE and babinski reflex
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27
Q

What’s babinski reflex associated with in adults

A

herniation of lower cervical disk, CNS disorder, spinal cord injury

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28
Q

TBI

A

alteration brain function or other evidence of brain pathology caused by external force

29
Q

Risk factors TBI

A
  1. falls children/elderly
  2. Men
  3. MVI
  4. American Indian and African American
30
Q

Types of primary brain injury (3)

A
  1. focal brain injury(closed brain injuries: epidural (extradural) hematoma, subderal hematoma, intracerebral hematoma)
  2. open brain injury
  3. diffuse brain injury
31
Q

S/S of contusion

A
  1. immediate LOC (last < 5 min)
  2. loss of reflexes (falls to ground)
  3. transient cessation of respiration
  4. brief bradycardia
  5. decrease BP (30 sec-few min)

Then everything returns to normal unless severe

32
Q

S/S epidural (extradural) hematoma

A

bleeding between dura mater & skull
1. LOC
2. increasing HA
3. vomiting
4. drowsiness
5. confusion
6. seizure
7. ipsilateral pupillary dilation
8. contralateral hemiparesis

33
Q

Early S/S acute subdural hematoma

A

bleeding between dura mater & arachnoid membrane covering brain; *most common cause intracranial mass
1. HA
2. drowsiness
3. restlessness/agitation
4. slowed cognition
5. confusion
**worsen over time

34
Q

Progressive s/s acute subdural hematoma

A
  1. LOC
  2. respiratory change
  3. pupillary dilation
  4. homonymous hemianopia (loss vision one eye)
  5. dysconjugate gaze
  6. gaze palsies
35
Q

S/S chronic subdural hematomas

A

chronic HA, tenderness over hematoma, progressive dementia w/ generalized rigidity (paratonia)

36
Q

s/s mild traumatic brain injury (mild concussion)

A

immediate but transitory clinical manifestations
1. No LOC or LOC < 30 min
2. GCS 13-15
3. confusion 1-several min
4. amnesia events preceding
5. HA
6. n/v
7. impaired concentration
8. difficulty sleeping

37
Q

s/s moderate traumatic brain injury (mod concussion)

A
  1. any LOC > 30 min-6 hours
  2. GCS 9-12
  3. maybe basal skull fx, no brainstem injury
  4. confused
  5. posttraumatic amnesia > 24 hours
  6. permanent deficits selective attention, vigilance, detection, working memory, data processing, vision/perception, language, mood/affect mild-severe
  7. *Abnormal brain imaging
38
Q

s/s severe traumatic brain injury (severe concussion)

A

permanent neuro; some vegetative/die

  1. LOC > 6 hours
  2. GCS 3-8
  3. brainstem damage signs: change pupillary reaction, cardiac/resp. sx, decorticate/decerebrate posturing, abnorm. reflexes
  4. brain imaging abnorm
  5. IICP 4-6 days after
  6. pulmonary, sensorimotor, cognitive
  7. compromised coordinated movements & communication, learn/reason, modulate behavior
39
Q

Goal of treating TBI

A

maintain cerebral perfusion/oxygenation, promote neuroprotection

40
Q

s/s postconcussion syndrome

A

weeks-months post mild concussion

HA
dizzy
fatigue
nervous/anxiety
irritable
insomnia
depression
inability to concentrate
forgetful

41
Q

chronic traumatic encephalopathy (CTE)

A

progressive dementing disease r/t repeated TBI (sports, soldiers); hydrophosphorylated tau neurofibrillary tangles
depression, suicide, memory, cognitive

42
Q

s/s sciatica

A

neurosensory/motor deficits
tingling/numb/weak parts leg/foot

43
Q

cauda equina syndrome

A

new onset b/b incontinence or urinary retention, loss of anal sphincter tone, saddle anesthesia
caused by herniated disk, tumor, infection, fracture, or narrowing of the spinal canal.

44
Q

s/s anterior cerebral artery stroke

A

contralateral leg more than arm weakness (hemiparesis)
minimal numbness
akinetic mutism (can’t move or speak) if bilateral vessel involve

45
Q

s/s middle cerebral artery stroke

A

contralateral (opposite side of body )Iupper limb more than leg weakness (hemiparesis) and numbness
ipsilateral (same side of body) hemianopsia and aphasia if stroke dominant hemisphere

46
Q

s/s posterior cerebral artery stroke

A

contralateral weakness and dizziness
hemianopsia
ataxia

47
Q

hemianopsia

A

blindness over half the field of vision

48
Q

s/s basilar artery stroke

A

difficult breathing
ataxia
nystagmus
vomiting
coma

49
Q

s/s cerebellar artery stroke

A

ataxia
vertigo
HA
n/v
slurred speech

50
Q

subarachnoid hemorrhage (SAH)

A

escape of blood from defective or injured vessel into subarachnoid space
Risk- aneurysm, family hx, HTN, HI

51
Q

s/s leaking vessel subarachnoid hemorrhage (early)

A

HA
change mental status/LOC
n/v
focal neuro deficits (weakness/paralysis, loss sensation, aphasia)

52
Q

s/s RUPTURED vessel subarachnoid hemorrhage

A

sudden explosive HA
n/v
visual disturbance
motor deficits
LOC
meningeal irritation/inflam. (neck stiff, blurred vision, photophobia, irritable, low-grade fever)
+Kernig
+brudzinski
seizures
hydrocephalus
hypothalamic dysfunction

53
Q

kernig sign

A

straightening the knee w/ hip/knee in flexed position produces pain in back and neck regions
*sign subarachnoid hemorrhage & meningitis

54
Q

brudzinski sign

A

passive flexion of neck produces neck pain and increased rigidity
*sign subarachnoid hemorrhage & meningitis

55
Q

s/s hypothalamic dysfunction in subarachnoid hemorrhage

A

salt wasting
hyponatremia
ECG change

56
Q

risk factors meningitis

A

otitis or sinusitis
immunocompromised
pneumonia

57
Q

s/s meningitis

A

fever, tachycardia, chills
throbbing HA
photophobia
nuchal rigidity
+kernig
+brudzinski
projectile vomit
decrease LOC
cranial nerve palsies
focal neuro deficits
***petechial/purpuric rash skin/mm

58
Q

purpura fulminans

A

in meningitis
rapid progressive syndrome of hemorrhagic infarction of skin and disseminated intravascular coag. lead to multi organ fail, ischemic necrosis of digits/limbs w/ amputation req., death
caused by bacterial endotoxin & inflammatory cytokines

59
Q

s/s HIV-associated neurocognitive disorder (HAND)

A

organic psychosis w/ agitation
inappropriate behavior
hallucinosis
difficulty speaking
progressive loss balance
gait disturb
paralysis

60
Q

what’s multiple sclerosis

A

immune-mediated inflammatory disease involving degeneration CNS myelin, scarring, loss axons

61
Q

s/s MS

A

paresthesias face, trunk, limbs
weakness
impaired gait
urinary incontinence
visual impairment
nystagmus
ataxia
weakness
tremor slurred speech

62
Q

Diffuse anoxal injury cause

A

traumatic shearing forces; tearing of axons from twisting/rotational forces w/ injury over widespread brain areas; moving head strikes hard, unyielding surface or moving object strikes stationary head; torsional head motion w/o impact

63
Q

s/s Diffuse anoxal injury

A

unconsciousness and persistent vegetative state after severe head trauma

64
Q

definition Diffuse anoxal injury (DAI)

A

involves widespread areas of brain, occurs w/ all severities of brain injury
coma > 6+ hours after TBI

65
Q

coma time mild diffuse anoxal injury (DAI)

A

6-24 hours

66
Q

coma time mod diffuse anoxal injury (DAI)

A

> 24 hours w/o abnormal posturing

67
Q

coma time severe diffuse anoxal injury (DAI)

A

> 24 hours w/ signs of brainstem involvement

68
Q

what does diffuse anoxal injury (DAI) do to brain

A

reduces speed of info processing & responding causes behavioral cognitive physical changes

69
Q

after effects diffuse anoxal injury (DAI)

A

NOT associated w/ intracranial HTN immediately after injury
acute brain swell by vasodilation, increase blood flow, cerebral blood volume can result in hypoxia-ischemia injury/death
long-term neurodegenerative processes (years)
develop chronic traumatic encephalopathy & Alzheimer disease-like pathologic changes

Pathophysiology (7 decks)

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