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Nursing School > Neuro > Flashcards

Neuro Flashcards

1
Q

Global ischemia

A

Blood flow cannot meet metabolic demands (cardiac arrest, shock, asphyxiation); ischemia to the entire brain

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2
Q

Focal ischemia

A

Ischemia to one focal or specific portion of the brain (strokes)

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3
Q

3 types of ischemic strokes

A
  1. thrombus (disease)
  2. Embolism (clots)
  3. Hypoxia (an event)
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4
Q

What is a hemorrhagic stroke

A

primary brain bleed

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5
Q

What do the vertebral arteries supply?

A

blood to brain stem, cerebella, and occipital lobes

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6
Q

What do the basilar and internal carotid arteries form?

A

Circle of Willis

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7
Q

Most common of the ischemic strokes

A

Thrombolytic strokes

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8
Q

Thrombolytic stroke caused by

A

build up of plaque, atherosclerosis

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9
Q

Clot originates somewhere in the body and travels to the brain

A

embolic stroke (detaches from primary site)

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10
Q

Causes of ischemic strokes

A

1.Atherosclerotic/cerebrovascular disease (narrow vessels, clots pass, thromboembolic)

  1. Cardiogenic source (afib and other arrhythmias, embolism dislodges)
  2. unusual causes
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11
Q

Large vessel thrombotic occlusions (LVO)/Strokes

A

occlusions that haven’t become embolic yet (not clots yet)

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12
Q

Most common large vessel thrombotic occlusion (LVO)

A

middle cerebral artery, anterior cerebral artery

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13
Q

Cerebral “Small vessel disease”/ thrombotic stroke

A

small and deep, linked to hypertension, likely a form of atherosclerosis, “white matter disease” on x-ray

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14
Q

Cerebral “small vessel disease” leading cause of…

A

loss of function, disability, cognitive decline (dementia, strokes, motor movement issues)

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15
Q

Transient ischemic attack (TCA)

A

short lived/passing/temporary form of ischemia. warning sign for stroke

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16
Q

Cardiogenic sources that can cause stroke

A

afib, MI, endocarditis, other dysrhythmias

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17
Q

Other unusual causes of strokes

A

vasospasm after subarachnoid hemorrhage, cerebral vasoconstriction syndrome, radiation therapy, air or fat embolism, amniotic fluid following birth, tumors

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18
Q

Tissue penumbra

A

tissue at risk for infarct if reperfusion does not happen fast

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19
Q

allows blood to seep into and damage brain tissues

A

hemorrhagic stroke

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20
Q

process of brain hemorrhage

A
  1. rupture of blood vessel
  2. bleeding goes to brain
  3. focal hematoma
  4. brain swells
  5. brain gets compressed
  6. coma/death
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21
Q

Symptoms of hemorrhagic stroke

A

“thunderclap headache”, contralateral hemiplegia (weakness on opposite side), spasticity (seizures), loss of consciousness, increased cranial pressure, coma/death

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22
Q

Causes and risk factors for what type of stroke…
- cardiovascular disease
- uncontrolled HTN
- heart disease/atherosclerosis
- diabetes
- afib
- CAD/stenosis
- hyperlipidemia
- obesity
- eclampsia during pregnancy

A

Ischemic stroke

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23
Q

Causes and risk factors for what type of stroke…
- uncontrolled HTN
- weak vessels/no clotting
- cerebral aneurysms
- arteriovenous malformations (twist)
- head trauma
- obesity
- smoking/alcohol
- drugs that spike BP (cocaine)
- women
- post-orgasm

A

hemorrhagic stroke

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24
Q

Primary injury of hemorrhagic stroke results from

A

compression by hematoma, ICP (intracranial pressure)

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25
Q

Secondary injury of hemorrhagic stroke if not treated

A

inflammatory response, disruption of blood brain barrier, cerebral edema, free radical overproduction, glutamate-induced excitotoxicity, release of hemoglobin and iron from clot

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26
Q

Two types of hemorrhagic stroke

A
  1. intracerebral hemorrhage
  2. subarachnoid hemorrhage
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27
Q

Intracerebral hemorrhage

A

deep penetrating vessels, injury to brain tissue by disrupting connecting pathways and causing localized pressure injury

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28
Q

Subarachnoid hemorrhage

A

intracranial bleeding into arachnoid and pia mater

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29
Q

What is the most common cause of intracerebral hemorrhage

A

uncontrolled hypertension

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30
Q

Most disabling and deadly kind of stroke

A

Intracerebral hemorrhage

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31
Q

ICH process

A
  1. ruptured vessel causes bleeding
  2. brain tissue lacks O2 and ATP
  3. constriction of blood leads to further decreased blood flow
  4. increases cranial pressure
  5. brain swells
  6. coma
  7. brain herniation
  8. death
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32
Q

Subarachnoid hemorrhage characteristics

A

ruptured vessel is slow, thunderclap headache, bleed into subarachnoid space, related to aneurysm, found near circle of willis

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33
Q

If a stroke occurs in left side of brain what can be affected

A

difficulty understanding spoken and written language, difficulty expressing spoken and written language, changes in speech, verbal memory issues, impaired logic, sequencing difficulties

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34
Q

If a stroke occurs in right side of brain what can be affected

A

attention, left side of body control, memory, decreased awareness of deficit, loss of “big picture” thinking, altered creative or music perception

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35
Q

One of the most dangerous strokes

A

brainstem stroke

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36
Q

Brainstem controls what vital functions

A

HR, lungs, breathing, swallowing, eye movement, facial movement/sensation, hearing

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37
Q

Cerebellum strokes can cause

A

ipsilateral motor symptoms (same side), problems with balance and coordination, dizziness/vertigo, nausea/vomiting, cognitive and mood symptoms

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38
Q

Warning signs of stroke
(BEFAST)

A

Balance, Eyes, Face, Arms, Speech, Time

numbness of face, arms, legs (one sided), sudden confusion, trouble speaking or understanding, trouble seeing, trouble walking, dizziness, loss of balance, sudden severe headache with no known cause

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39
Q

Aphasia

A

absence of ability to communicate with words from damage to brain

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40
Q

Wernicke’s aphasia

A

fluent aphasia, full sentences that make no sense (word salad); reading and writing severely impaired

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41
Q

Broca’s aphasia

A

nonfluent aphasia, person understands language but has difficulty getting their own words out (expressive aphasia), may be able to read and write

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42
Q

global aphasia

A

most severe of aphasias, produce few recognizable words and understands little to no language

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43
Q

Primary progressive aphasia (PPA)

A

neurodegenerative disorder causing slow progression form of aphasia that worsens over time (alzheimers)

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44
Q

Abnormal pupillary responses

A

unilateral dilation (compression of nerve CN 3), constricted pupils, bilateral, fixed and dilated (serious brain damage)

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45
Q

NIH stroke scale

A

0 - no stroke symptoms
1-4 - minor stroke
5-15 - moderate stroke
16-20 - moderate to severe stroke
21-42 - severe stroke

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46
Q

Glasgow coma scale

A

Measures alertness
13-15 - minor
9-12 - moderate
8 or lower - severe

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47
Q

Stroke treatment: Ischemic

A

restore perfusion via Tissue plasminogen activator (t-PA), surgical intervention (thrombectomy)

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48
Q

Stroke treatment: Hemorrhagic

A

stop/control bleeding, remove hematoma, brain drain post craniotomy, burr holes, BP control, manage ICP

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49
Q

What does t-PA do

A

breaks up clot; converts plasminogen to the proteolytic enzyme plasmin, which lyses fibrin as well as fibrinogen

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50
Q

Window of opportunity for reperfusion for ischemic stroke

A

4 hours for optimal outcomes from tPA

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51
Q

Questions to ask before use of t-PA

A

confirm that the stroke is ischemic (NOT hemorrhagic), any history of cerebral hemorrhage or head trauma, recent bleeds, recent surgery, history of stomach ulcer/GI bleed, uncontrolled HTN, thrombocytopenia, seizure disorder, advanced age

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52
Q

CNS consists of

A

brain, spinal cord

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53
Q

PNS consists of

A

cranial nerves, spinal nerves

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54
Q

Afferent pathway

A

incoming sensory pathways to brain

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55
Q

Efferent pathway

A

outgoing motor pathways to body

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56
Q

Functioning cells of the nervous system, responsible for transport and uptake of neurotransmitters

A

neuron

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57
Q

class of cells that protects and provides developmental, physiological, and metabolic support for neurons, capable of mitosis, astrocytes, oligodendrocytes, microglia

A

neuroglia (glial cells)

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58
Q

Provide nutrients and structure for synapses, regulate ion and chemical concentrations, form blood brain barrier

A

astrocytes (CNS)

59
Q

Myelinates CNS cells, enables fast propagation of action potentials along axons

A

oligodendrocytes (CNS)

60
Q

critical for CSF homeostasis, brain metabolism, and clearance of waste from brain

A

ependymal cells (CNS)

61
Q

degrade dead cells and protect the brain from invading microorganisms

A

microglia (CNS)

62
Q

surround neuron cell bodies in PNS

A

satellite cells

63
Q

surround all nerve fibers in PNS and form myelin sheaths around nerve fibers

A

Schwann cells

64
Q

Carry signals from outer parts of body (periphery) into CNS, dendrites on both ends connected by long axon with cell body in middle

A

sensory neurons

65
Q

control muscle contractions have cell body on one end, long axon in middle and dendrites on other end, carry signals from CNS to body

A

Motor neurons

66
Q

amount of work required to separate + and - charged particles that are attracted to eachother

A

electrical potential

67
Q

cell at “rest” before any stimulation (negative at rest)

A

resting potential

68
Q

when membrane becomes less negative, more likely to fire

A

depolarization

69
Q

resting potential becomes more negative, less likely to fire

A

hyperpolarization

70
Q

temporary shift from negative to positive in neurons membrane potential caused by ions suddenly

A

action potential

71
Q

currents that prompt one neuron to share information with next through action potential

A

excitatory current

72
Q

level that a depolarization must reach for an action potential to occur

A

threshold of excitation

73
Q

monroe-kellie doctrine

A

states that the sum of these volumes (brain, CSF, intracranial blood) should be constant, increase in one should cause a decrease in on or both remaining two
V intracranial volume = V brain. matter + V CSF + V blood

74
Q

Factors that can cause increased ICP

A

hematoma, tumor, abscesses, infarcts, hydrocephalus, meningitis, increase in blood volume (acidosis causes increase CO2 and leads to increase cerebral blood flow), aneurysms, head trauma, venous stasis from thrombus, skull deformity, TBI

75
Q

Early signs and symptoms of increased ICP

A

LOC, restless, pupillary changes (ovoid), headache, speech (slurring), decreased motor function, GI problems

76
Q

Late signs and symptoms of increased ICP

A

LOC, pupillary changes (dilation, pupilledema, swelling of optic nerve), vital sign changes, abnormal reflexes, loss of brainstem reflex (sluggish then loss of corneal, cough, gag), pathologic posturing (decorticate and decerebrate)

77
Q

Decorticate posture

A

closed hands, legs internally rotated, feet inward, arms are adducted and flexed against chest

78
Q

Decerebrate posturing

A

head and neck arched, legs straight, toes pointed down, arms straight and extended with hands curled

79
Q

Cushing’s triad

A

sign of cerebral swelling resulting from trauma or a space occupying lesion that is growing, posing impending fatal herniation of brain
1. change in respirations (deep and irregular)
2. widening pulse pressure (big difference in systolic and diastolic)
3. bradycardia

80
Q

What happens when increased ICP is untreated

A

herniation of brain and death

81
Q

Traumatic brain injuries (TBI)

A

concussion, contusion, coup contrecoup, diffuse axonal injury, chronic traumatic encephalopathy, second impact syndrome, traumatic hemorrhage, subarachnoid hemorrhage (not stroke)

82
Q

Mild form of TBI, by impact to the head or whiplash

A

concussion

83
Q

bruises on specific brain areas from impact to head

A

contusion

84
Q

contusion present at both the site of impact and the exact opposite end of impact

A

coup contrecoup

85
Q

shearing (tearing) of brain’s long connecting nerve fibers (axons) that happens when brain is injured as it shifts and rotates inside bony skull, usually causes coma and injury, may have normal CT

A

Diffuse axonal injury

86
Q

brain degeneration likely caused by repeated head traumas, made only at autopsy by studying sections of brain

A

Chronic traumatic encephalopathy (CTE)

87
Q

repetitive head injury syndrome, condition in which individual experiences a second head injury before complete recovery from initial head injury

A

second impact syndrome (SIS)

88
Q

TBI : hematoma (bleeding outside brain or even inside that is NOT CVA) what are the two types

A

Epidural, subdural

89
Q

arterial bleed, high pressure bleed fast, most dangerous, bleeding above dura, leads to increase ICP

A

characteristics of epidural hematoma

90
Q

venous bleed, low pressure bleed, subdural space, leads to increase ICP

A

characteristics of subdural hematoma

91
Q

Subarachnoid hemorrhage (SAH not stroke)

A

small arteries tear during initial injury, pathologic presence of blood in subarachnoid space, second most common acute injury

92
Q

Sign of most severe TBI

A

increased ICP

93
Q

TBI categorized by severity and mechanism of injury…what are these rankings

A

severe: unconscious, eyes dont open, LOC > 6 hrs

moderate: lethargic, open eyes to stimuli, LOC 20 min-6 hrs, brain swelling

mild: awake, eyes open, confusion, disorientation, memory loss, headache, brief LOC

94
Q

Side effects of TBI physical symptoms

A

LOC from mins-hrs, persistent headache or headache that worsens, nausea, vomiting, convulsions or seizures, dilation of one or both pupils, clear fluids draining from nose or ears, inability to wake from sleep

95
Q

Which one…Cognitive/behavioral/mental or sensory symptoms of TBI
- burred vision, ringing in ears, bad taste in mouth or changes of ability to smell, sensitivity to light or sound

A

sensory symptoms of TBI

96
Q

Cognitive/behavioral/mental or Sensory symptoms of TBI
- LOC from secs-hrs, dazed, confused, disoriented, memory or concentration problems, mood changes or mood swings, depressed or anxious, difficulty sleeping, sleeping more

A

Cognitive, behavioral, mental symptoms of TBI

97
Q

Frontal lobe deals with

A

concentration, problem solving, speech

98
Q

Parietal lobe deals with

A

sense of touch, pain, temperature

99
Q

Occipital lobe deals with

A

healthy vision

100
Q

Temporal lobe deals with

A

memory, organization

101
Q

Cerebellum deals with

A

balance and coordination

102
Q

Brainstem deals with

A

breathing, steady heart rate

103
Q

How can a TBI affect areas of the brain

A

Frontal: lack of focus, irritability, language difficulty
Parietal: difficulty w/reading, spatial misperception
Occipital: blind spots, blurred vision
Temporal: problems w/short term and long term memory
Cerebellum: difficulty walking
Brainstem: changes in breath, difficulty swallowing

104
Q

Who is at risk for a spinal cord injury

A

males and ages 16-30

105
Q

Impacts of SCI (spinal cord injury)

A

Physical dependency, morbidity/mortality, physiological stress, financial burden

106
Q

Cascade of destructive events of SCI

A

ischemia, oxidative stress, inflammatory events, apoptotic pathways

107
Q

Outcomes of spinal cord injury

A

incomplete quadriplegia (weakness or paralysis of all 4 limbs)

complete paraplegia (complete cut off of connection from brain and area below injury)

complete quadriplegia (neck down is affected)

incomplete paraplegia (not completely severed cords )

108
Q

3 primary roles of spinal cord

A

send motor commands from brain to body, send sensory information from body to brain, coordinate reflexes

109
Q

A spinal cord injury that disrupts conduit between body and brain and can lead to deficits in

A

sensation, movement, autonomic regulations, death

110
Q

Where does the spinal tract begin and end

A

begins at brain (foramen magnum) and terminates at L1-L2

111
Q

Ascending tract sends information…

A

sensory information to the brain

112
Q

Descending tracts send information…

A

motor information down the cord

113
Q

Complete SCI

A

all feeling/sensory input and all motor control/movement/function are lost below the level of injury

114
Q

Incomplete SCI

A

some motor or sensory function loss below the affected area are preserved

115
Q

Paraplegia paralysis

A

affects all or part of the trunk, legs, and pelvic organs (below waist), may still have movement of upper limbs

116
Q

Tetraplegia/quadriplegia

A

arms, hands, trunk, legs, and pelvic organs are all affected by the injury (neck down)

117
Q

what might happen to a person if they have a C1-C4 injury

A

may not be able to breathe on their own

118
Q

Brown sequard syndrome

A

ipsilateral weakness/paralysis, contralateral sensory loss of pain and temperature below level of injury, usually puncture can be infectious or MS

119
Q

Central cervical cord syndrome

A

impacts upper limbs more than lower, severe arm weakness, sensory deficits variable, caused by hyperextension of neck, compression, squash of spinal cord

120
Q

Posterior cord syndrome

A

decrease in sensation of fine touch, loss of balance/coordination (+ Romberg), SCI, demyelinating disorders, compression from tumor, or degenerative disorder

121
Q

Anterior cord syndrome

A

motor paralysis below level of lesion, loss of pain sensation below injury, SCI, severe loss of blood, trauma, affects anterior 2/3 of spinal cord

122
Q

Which spinal cord syndrome causes poorest outcome

A

anterior cord syndrome

123
Q

SCI shocks

A

normal activity of spinal cord cells cease at and below level of injury

124
Q

Spinal shock

A

complete loss of reflex function, flaccid paralysis, sensory deficit, loss of bladder and rectal control, drop in BP and poor circulation, loss of thermal control, resolve when reflexes return, lower spinal cord level T7 or below

125
Q

Neurogenic shock

A

sudden loss of sympathetic nervous system that maintains normal vascular tone, blood volume not impaired but is displaced producing hypotensive state and bradycardia, massive vasodilation, T6 and above

126
Q

either in motor cortex of brain or brainstem, initiate voluntary movement throughout the body by connecting the cerebral cortex to the brain stem and spinal cord, sends nerve impulses from the brain to lower motor neuron synapses

A

Upper motor neurons (UMN)

127
Q

neurons which travel from the spinal cord to the muscles of the body, directly responsible for communicating signals to the skeletal muscles, organs and glands, sends nerve impulses from upper motor neurons to the muscles via the lower motor neurons

A

Lower motor neurons (LMN)

128
Q

Where are Upper motor neuron disorders located

A

central nervous system (CNS)

129
Q

Where are the lower motor neuron disorders located

A

spinal cord grey matter or within the cranial nerve nuclei in the brains tem

130
Q

What type of motor neuron disorders are these…
ALS, TBI, spinal cord injury, MS, CVAs (cerebrovascular accident), huntington’s disease

A

Upper motor neuron disorder

131
Q

What type of motor neuron disorders are these…
poliomyelitis, spinal muscular atrophy SCI (spinal cord injury) can impact both

A

lower motor neuron disorder

132
Q

What goes on in the body after an upper motor neuron lesion

A

spastic hyperreflexia, muscle weakness

133
Q

What goes on in the body after a lower motor neuron lesion

A

muscular atrophy, flaccid muscle weakness, fasciculation (twitch) and hyporeflexia

134
Q

Progressive and potentially disabling disease of the brain and spinal cord characterized by destruction of the myelin sheaths on the neurons of the CNS

A

Multiple Sclerosis

135
Q

Causes of MS

A

largely unknown, auto immune disease, possibly environmental, genetic susceptibility

136
Q

Pathogenesis of MS

A

T-cells attack myelin sheath as if it were a pathogen, demyelination occurs, damages action potential between axons on neurons

137
Q

Neurodegenerative disorder that primarily affects the motor system and presents with progressive muscle weakness, both upper and lower motor neurons impacted

A

ALS (amyotrophic lateral sclerosis)

138
Q

Early signs of ALS

A

split hand syndrome, foot drop, wasting of tongue muscle, uncontrolled laughter/crying, muscle cramps and twitches, dysphagia, slurred speech, impaired fine motor control

139
Q

Late signs of ALS

A

diffuse severe muscle weakness, diffuse muscle atrophy, problems w/movement, dysphagia, problems speaking, impaired breathing

140
Q

Generalized acetylcholine receptor (AChR) myasthenia

A

chronic autoimmune disease, antibodies destroy communication between nerves and muscle resulting in weakness of skeletal muscles

141
Q

Neonatal myesthenis

A

temporary form in fetus of myasthenia gravis patient, passes acetylcholine receptor through placenta

142
Q

Ocular myasthenia

A

muscles that move the eyes and control the eyelids are easily fatigued and weakened

143
Q

Clinical manifestations of myasthenia gravis

A

usually affects women in 20-30 and men 50-60, drooping of eyelid (ptosis), weak eye and face muscles, impaired speech (dysarthria), dysphagia, weakness

Nursing School (9 decks)

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