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Pathophysiology > Exam 4 - Concepts Of Neurologic Dysfunction > Flashcards

Exam 4 - Concepts Of Neurologic Dysfunction Flashcards

1
Q

What controls the blood flow to the brain?

A

Baroreceptors in the carotid arteries

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2
Q

What is the Monroe Kellie Doctrine?

A

A theory that says there is only so much room in the head. So when new things are added, things spill over

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3
Q

What happens if something extra is added to the head?

A

1 - CSF gets pushed down into subarachnoid space
2 - Blood is pushed down to venous sinuses
3 - Brain tissue moves (herniation)

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4
Q

What is herniation?

A

Tissue movement

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5
Q

What does herniation cause?

A

Decreased LOC
Neurologic changes
Leads to death

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6
Q

Normal MAP

A

70-90

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7
Q

To prevent brain anoxia, what must MAP be?

A

> 60

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8
Q

Normal intracranial pressure

A

0-15

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9
Q

What does ICP need to be to lead to herniation?

A

> 20 for 5 minutes or more

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10
Q

What does CPP stand for?

A

Cerebral profusion pressure

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11
Q

Formula for CPP

A

CPP = MAP - ICP

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12
Q

How do we measure ICP when determining CPP?

A

Can estimate it

To know true amount, need to measure by probe in head

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13
Q

What type of values are MAP and ICP?

A

Trend values

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14
Q

Measurement to determine if we need to act on MAP or ICP

A

> 5 pressure changes in 25 minutes

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15
Q

What is auto regulation?

A

Compensatory mechanism (normal body function)

Controls constriction and dilation of blood vessels in the head

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16
Q

What happens during autoregulation if a patient has high blood pressure?

A

Carotids alert vessels in head to constrict

Vessels in rest of body would dilate

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17
Q

What would happen with autoregulation if a patient had low blood pressure?

A

Carotids would cause vessels in head to dilate

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18
Q

What would you, as a nurse, do for a patient with low blood pressure and a high heart rate?

A

Give patient fluids

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19
Q

What do vasodilators do in regards to autoregulation?

A

Cause vessels throughout body to dilate

But do not affect autoregulation

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20
Q

What does bruit do to baroreceptors in the carotids?

A

Disables the baroreceptors and prevents them from autoregulating

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21
Q

What is accommodation?

A

Compensatory mechanism (normal body function)

Downward movement of contents in head. The contents move/change according to need

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22
Q

What compensatory mechanism occurs when a patient has hypercapnia?

A

Autoregulation

Carotids send signal for vessels in brain to dilate so brain can get more O2

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23
Q

What compensatory mechanism occurs when a patient has hyperoxygenation?

A

None

Autoregulation will not respond

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24
Q

What is a jugular obstruction?

A

An obstruction in jugular vein or carotids that cuts of circulation to brain

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25
Q

Examples of things that can cause a jugular obstruction

A

Hyperextending carotids

Coughing
Vomiting
Bearing down

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26
Q

How does coughing, vomiting, or bearing down cause a jugular obstruction?

A

Changes the thoracic pressure

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27
Q

What happens to carotids when someone has a jugular obstruction?

A

Circulation to brain is cut off

Blocks carotids’ ability to auto regulate

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28
Q

Examples of conditions that would make the body need more oxygen

A 
Seizure
High temperature
Shivering
Pain
Stimulants
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29
Q

What happens to the carotids if body needs more oxygen?

A

Carotids cause dilation to autoregulate

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30
Q

What is the only thing that can cause carotids to not be able to auto regulate anymore?

A

Obstruction (heard as bruit)

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31
Q

What is arousal?

A

State of awareness

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32
Q

What is a vegetative state?

A

Loss of cerebral function (minimal function of brain)

Crude awakened state

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33
Q

What would someone in a vegetative state be able to do?

A

Awake
May be able to make eye contact
May be able to swallow
Vitals, cardiac and respiratory systems intact

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34
Q

What is content of thought?

A

Encompasses moods (a patient’s mood/emotional intelligence)

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35
Q

Example of assessing a patient’s content of thought

A

Do this while assessing LOC

Asking them what day it is, etc

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36
Q

Tool used to diagnose a patient’s LOC

A

Glasgow coma scale

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37
Q

What is the Glasgow Coma Scale?

A

15 point scale

Assesses level of consciousness by considering three areas

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38
Q

Three areas of the Glasgow Coma Scale

A

Eye opening
Motor response
Verbal response

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39
Q

Explain the scoring of the Glasgow Coma Scale

A

Scored on a scale of 0-15
15 = highest, 0 = dead

0-3 = coma
3-8 = severe injury
9-15 = injury is not as severe
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40
Q

What is the main score of a Glasgow Coma Scale we should be concerned with?

A

3 - 8, which means severe injury

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41
Q

Most critical index of nervous system function

A

Level of consciousness

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42
Q

What is a LOC with highest level of functioning?

A

Alert and oriented to self, others, place, time, and situation

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43
Q

What should always be the number one priority?

A

LOC

The other symptoms come later

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44
Q

What is the first symptom when someone suffers a head injury?

A

LOC

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45
Q

LOC is the only sign for what?

A

Of perfusion

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46
Q

Loss of ability to think rapidly and clearly

Impaired judgement and decision making

A

Confusion

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47
Q

Beginning loss of consciousness

A

Disorientation

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48
Q

If someone is disoriented, what is the order of orientation that they will lose?

A

Time
Place and impaired memory
Recognition of self

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49
Q

Limited spontaneous movement or speech

A

Lethargy

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50
Q

Easy arousal with normal speech or touch

A

Lethargy

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51
Q

What is person with lethargy oriented to?

A

May or may not be oriented to time, place, or person

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52
Q

Mild to moderate reduction in arousal with limited response to the environment

A

Obtundation

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53
Q

Person falls asleep unless stimulated verbally or tactilely

A

Obtundation

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54
Q

Answers questions with minimum response

A

Obtundation

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55
Q

Condition of deep sleep or unresponsiveness

A

Stupor

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56
Q

Person may be aroused from deep sleep or open eyes only by vigorous and repeated stimulation

A

Stupor

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57
Q

Pt response when stimulated is often withdrawal or grabbing at stimulus

A

Stupor

58
Q

No verbal response to external environment or to any stimuli

A

Coma

59
Q

Pain or suctioning do not yield motor movement

A

Coma

60
Q

If patient has brain death

A

Complete death of brain, including brain stem
No recovery
Unable to maintain body’s internal homeostasis

61
Q

If patient has cerebral death

A

Brain stem does work
Internal homeostasis intact
Irreversible coma
Permanent brain damage

62
Q

What does a patient with cerebral death act like?

A

Doesn’t respond to stimuli
Can’t follow commands
Can’t swallow = at big risk for aspiration

63
Q

What are the determinants of brain death?

A

1- Completion of all appropriate and therapeutic procedures
2- Unresponsive coma (no motor or reflex movements)
3- No spontaneous respiration
4- No ocular responses to head turning or caloric stimulation; dilated, fixed pupils
5- Isoelectric (flat) EEG = electrocerebral silence

64
Q

How long do these signs need to persist for to determine brain death?

A

30 mins to 1 hour

And for 6 hours after onset of coma and apnea

65
Q

What is an optional test that can be added as a determinant of brain death?

A

Confirming test indicating absence of cerebral circulation

66
Q

How long is an EEG used for to detect brain waves while determining if pt has brain death?

A

24 hours

67
Q

If pt has slowing brain waves seen on EEG, what is needed to be done?

A

Test blood flow

Can be done through IV contrast test to look for decreased circulation

68
Q

3 main things to determine brain death

A

1 - EEG - detect brain waves
2 - if slowed brain waves, test blood flow
3 - need to do one additional bedside exam

69
Q

3 exams that can be done as the additional bedside exam when determining brain death

A

Babinski
Occulocephalic
Occulovestibular response

70
Q

What is a seizure?

A

Sudden, explosive, disorderly discharge of cerebral neurons

With sudden transient alteration in brain function

71
Q

What compensatory mechanism occurs when a patient has a seizure?

A

Autoregulation

72
Q

Types of dysfunction that seizures cause

A

Motor
Sensory
Autonomic
Psychic

73
Q

What is a convulsion?

A

Jerky, contract-relax (tonic-clonic) movement associated with seizures

74
Q

What is epilepsy?

A

Seizure with no underlying correctable cause

75
Q

In general, what causes seizures?

A

Any disorder that alters neuronal environment

76
Q

Possible etiology of seizure activity

A
  • Cerebral lesions (tumors)
  • Biochemical disorders
  • Cerebral trauma (injury)
  • Epilepsy
77
Q

Examples of biochemical disorders that cause seizure activity?

A

Schizophrenic
Manic/depressive
Severe hyponatremia

78
Q

Top Risk Factors of seizure activity

A

Infection; fever
Brain tumor
Vascular disease (AV valve dysfunction)
Drug or alcohol abuse

79
Q

Other Risk Factors of seizures

A
  • Metabolic defects
  • Congenital, genetic, perinatal injury
  • Postnatal injury
  • Myoclonic syndromes
80
Q

What metabolic defect causes seizures?

A

Not enough bicarbonate produced by the kidneys

Causes build up of acid

81
Q

What can seizures be precipitated by?

A 
Fatigue; lack of sleep
Emotional of physical stress
Febrile illness
Large amounts of water ingestion
Constipation
Drugs
Hyperventilation
Environmental stimulants
82
Q

Why does water intoxication precipitate seizures?

A

ADH malfunction

83
Q

Which drugs can precipitate seizures?

A

Stimulants

Withdrawal of antidepressants

84
Q

Environmental stimulants that can precipitate a seizure

A

Blinking lights

Loud noises

85
Q

Types of epileptic seizures

A

Partial (AKA focal or simple)
Complex (AKA psychomotor or temporal lobe)
Secondarily generalized
Generalized

86
Q

What occurs with a partial seizure?

A

Not full body

No loss of consciousness, can communicate with eyes

87
Q

What happens with a complex seizure?

A

Not full body

Impaired consciousness

88
Q

What happens with a secondarily generalized seizure?

A

Smaller focal seizure that evolves to generalized

89
Q

What is a generalized seizure?

A

Full body seizure

90
Q

Types of generalized (full body) seizures

A

Petit mal
Grand mal
Drop attack (AKA atonic)

91
Q

What is a petit mal seizure?

A

Small version of a total body seizure

92
Q

Types of petit mal seizures

A

Absence
Myoclonic
Clonic
Tonic

93
Q

What is an absence petit mal seizure?

A

No visible symptoms, person stares ahead

94
Q

What is a myoclonic petit mal seizure?

A

Mixture of tonic and clonic in one seizure

95
Q

What does clonic petit mal seizure mean?

A

Relaxation

96
Q

What does tonic petit mal seizure mean?

A

Stiffness

97
Q

What is a grand mal seizure?

A

Big seizure

Patient has both tonic and clonic movement

98
Q

What is a drop attack?

A

Seizure where person stiffens and falls over

99
Q

What is an aura?

A

Partial seizure (partial state of awareness) preceding onset of generalized seizure

100
Q

Description of an aura

A

Can be gustatory, visual, or auditory

Can experience dizziness, numbness, or a “funny feeling”

101
Q

What is prodroma?

A

A very early sign/symptom that a person will have a seizure. Occurs hours or days before a seizure

102
Q

What does a person feel like while experiencing prodroma?

A

Malaise
Headache
Sense of depression

103
Q

Definition of tonic

A

State of muscle contraction with excessive tone (prolonged)

104
Q

Definition of clonic

A

State of alternating contraction with relaxation of muscles (usually rapid)

105
Q

What is a postictal phase?

A

Time period immediately following the cessation of seizure activity

106
Q

How long does the postictal phase last?

A

Minutes to hours, to a day or longer

107
Q

What does a person in the postictal phase feel like? And why?

A

Exhausted
Because seizure had high O2 demand and used a lot of glucose
May have migraine or incontinence

108
Q

*Nursing considerations for a client with seizure activity

A
  1. No hands in mouth
  2. No tongue blades
  3. Bed in lowest position
  4. Bed side rails up
  5. Wrap padding around side rails
  6. Put mattress on floor for patient to lay on
109
Q

*How to document a seizure

A
  1. When it started
  2. When it ended
  3. How long it lasted
  4. Describe postictal phase
  5. Any injuries?
110
Q

Definition of dementia

A

Long-term progressive failure of many cerebral functions

*NOT caused by impaired LOC

111
Q

Clinical manifestations of dementia

A

Decreased:

  • Orientation
  • Recent memory (1st to go)
  • Remote memory (happens much later)
  • Language affected
  • Executive networks (entire thought process eventually affected)
112
Q

Can dementia kill a person?

A

No, they eventually wither away

113
Q

Leading cause of sever cognitive dysfunction in older adults

A

Alzheimer disease

114
Q

What does Alzheimer disease cause?

A

Atrophy of brain and loss of neurons

115
Q

How is Alzheimer disease diagnosed?

A

By exclusion, based on clinical findings
(Must exclude other issues before diagnosing. This is time consuming and expensive, so often doctors just guess that a pt has Alzheimer’s)

Usually don’t know for sure until death and an autopsy is done

116
Q

How long does Stage 1 of Alzheimer Disease last?

A

2-4 years

117
Q

Clinical manifestations of Stage 1 of Alzheimer disease

A

Memory loss
Subtle personality changes
Disorientation to time and place

118
Q

What is stage 2 of Alzheimer disease called?

A

Confusion stage

119
Q

How long does Stage 2 of Alzheimer disease last?

A

Several years

120
Q

Clinical manifestations of Stage 2 of Alzheimer disease

A 
Impaired cognition
Restlessness
Agitation
Wandering
Sundowner’s syndrome
Repetitive behavior
121
Q

What is sundowner’s syndrome?

A

Up all night and sleep all day

Wander around during night

122
Q

What is Stage 3 of Alzheimer disease called?

A

Terminal stage

123
Q

How long does Stage 3 of Alzheimer disease last?

A

1-2 years

124
Q

Clinical manifestations of Stage 3 of Alzheimer disease

A

Emancipation
Inability to communicate
Bowel and bladder incontinence
Seizures

125
Q

Definition of hydrocephalus

A

Excess fluid in cranial vault

In subarachnoid space or both

126
Q

Cause of hydrocephalus

A

Increased fluid production

Or defective reabsorption of fluid

127
Q

Types of hydrocephalus

A

Noncommunicating - obstruction in draining pathway

Communicating - defective absorption

128
Q

Clinical manifestations of hydrocephalus

A 
Unsteady, broad-based gait
History of falls
Apathy
Inattentiveness 
Indifference to self, family, and environment

In infant - large head

129
Q

If an adult has hydrocephalus, skull can’t move, so what occurs in head?

A

Accommodation

130
Q

How can chronic hydrocephalus be treated for an adult?

A

EVD (electro ventricular device)

Pulls CSF out and drops it back into circulation

131
Q

Definition of paresis

A

Weakness and partial paralysis

With incomplete loss of muscle power

132
Q

Definition of paralysis

A

Loss of motor function

133
Q

Weakness on one side of the body (spelling)

A

Hemiparesis

134
Q

Paralysis on one side of the body (spelling)

A

Hemiplegia

135
Q

Paralysis of both upper and lower extremities (spelling)

A

Diplegia

136
Q

Paralysis of lower extremities (spelling)

A

Paraplegia

137
Q

Paralysis of all four extremities (spelling)

A

Quadriplegia

138
Q

Definition of Parkinson disease

A

Degenerative disorder of basal ganglia function

139
Q

What is Parkinson disease characterized by?

A

Progressive destruction of nigrostriatal pathway

Subsequent reduction striata concentrations of *dopamine

140
Q

Cardinal manifestations of Parkinson disease

A

Tremor
Rigidity
Bradykinesia (slowness of movement)

Pathophysiology (14 decks)

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