Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

Chapter 17- Central & Peripheral Nervous Systems Flashcards

(69 cards)

Start Studying
1
Q

primary spinal cord injury

A

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

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

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

Ex secondary spinal cord injuries

A

hemorrhages, inflammation, edema, ischemia

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

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

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

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

Most common areas for vertebral injuries in adults

A

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

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

Spinal shock

A

temporary loss of spinal cord functions below lesion immediately after injury

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

causes of spinal shock

A

cord hemorrhage, edema, or anatomic transection

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

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

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

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

Who is at risk for neurogenic shock

A

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

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

S/S neurogenic shock

A
  1. vasodilation
  2. hypotension
  3. bradycardia
  4. failure of body temp regulation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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

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

What can dysreflexia lead to if untreated

A

stroke, seizure, MI, death
requires immediate tx

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

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

Most common cause dysreflexia

A

1 distended bladder or rectum

any sensory stim. can cause

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

What’s herniated disc

A

displacement of nucleus pulposus or annulus fibrosus beyond intervertebral disk space

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

Where does disc herniation usually occur

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Clinical manifestation herniated dic lumbarsacral region
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
26
Clinical manifestation herniated dic lower cervical region
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
27
What's babinski reflex associated with in adults
herniation of lower cervical disk, CNS disorder, spinal cord injury
28
TBI
alteration brain function or other evidence of brain pathology caused by external force
29
Risk factors TBI
1. falls children/elderly 2. Men 3. MVI 4. American Indian and African American
30
Types of primary brain injury (3)
1. focal brain injury(closed brain injuries: epidural (extradural) hematoma, subderal hematoma, intracerebral hematoma) 2. open brain injury 3. diffuse brain injury
31
S/S of contusion
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
S/S epidural (extradural) hematoma
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
Early S/S acute subdural hematoma
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
Progressive s/s acute subdural hematoma
1. LOC 2. respiratory change 3. pupillary dilation 4. homonymous hemianopia (loss vision one eye) 5. dysconjugate gaze 6. gaze palsies
35
S/S chronic subdural hematomas
chronic HA, tenderness over hematoma, progressive dementia w/ generalized rigidity (paratonia)
36
s/s mild traumatic brain injury (mild concussion)
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
s/s moderate traumatic brain injury (mod concussion)
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
s/s severe traumatic brain injury (severe concussion)
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
Goal of treating TBI
maintain cerebral perfusion/oxygenation, promote neuroprotection
40
s/s postconcussion syndrome
weeks-months post mild concussion HA dizzy fatigue nervous/anxiety irritable insomnia depression inability to concentrate forgetful
41
chronic traumatic encephalopathy (CTE)
progressive dementing disease r/t repeated TBI (sports, soldiers); hydrophosphorylated tau neurofibrillary tangles depression, suicide, memory, cognitive
42
s/s sciatica
neurosensory/motor deficits tingling/numb/weak parts leg/foot
43
cauda equina syndrome
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
s/s anterior cerebral artery stroke
contralateral leg more than arm weakness (hemiparesis) minimal numbness akinetic mutism (can't move or speak) if bilateral vessel involve
45
s/s middle cerebral artery stroke
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
s/s posterior cerebral artery stroke
contralateral weakness and dizziness hemianopsia ataxia
47
hemianopsia
blindness over half the field of vision
48
s/s basilar artery stroke
difficult breathing ataxia nystagmus vomiting coma
49
s/s cerebellar artery stroke
ataxia vertigo HA n/v slurred speech
50
subarachnoid hemorrhage (SAH)
escape of blood from defective or injured vessel into subarachnoid space Risk- aneurysm, family hx, HTN, HI
51
s/s leaking vessel subarachnoid hemorrhage (early)
HA change mental status/LOC n/v focal neuro deficits (weakness/paralysis, loss sensation, aphasia)
52
s/s RUPTURED vessel subarachnoid hemorrhage
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
kernig sign
straightening the knee w/ hip/knee in flexed position produces pain in back and neck regions *sign subarachnoid hemorrhage & meningitis
54
brudzinski sign
passive flexion of neck produces neck pain and increased rigidity *sign subarachnoid hemorrhage & meningitis
55
s/s hypothalamic dysfunction in subarachnoid hemorrhage
salt wasting hyponatremia ECG change
56
risk factors meningitis
otitis or sinusitis immunocompromised pneumonia
57
s/s meningitis
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
purpura fulminans
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
s/s HIV-associated neurocognitive disorder (HAND)
organic psychosis w/ agitation inappropriate behavior hallucinosis difficulty speaking progressive loss balance gait disturb paralysis
60
what's multiple sclerosis
immune-mediated inflammatory disease involving degeneration CNS myelin, scarring, loss axons
61
s/s MS
paresthesias face, trunk, limbs weakness impaired gait urinary incontinence visual impairment nystagmus ataxia weakness tremor slurred speech
62
Diffuse anoxal injury cause
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
s/s Diffuse anoxal injury
unconsciousness and persistent vegetative state after severe head trauma
64
definition Diffuse anoxal injury (DAI)
involves widespread areas of brain, occurs w/ all severities of brain injury coma > 6+ hours after TBI
65
coma time mild diffuse anoxal injury (DAI)
6-24 hours
66
coma time mod diffuse anoxal injury (DAI)
> 24 hours w/o abnormal posturing
67
coma time severe diffuse anoxal injury (DAI)
> 24 hours w/ signs of brainstem involvement
68
what does diffuse anoxal injury (DAI) do to brain
reduces speed of info processing & responding causes behavioral cognitive physical changes
69
after effects diffuse anoxal injury (DAI)
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)

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