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Pathophysiology > Ch. 11 Neural Function > Flashcards

Ch. 11 Neural Function Flashcards

1
Q

what are the causes of neural disorders?

A

congenital defects, trauma, infections, tumors, chemical imbalances, and vascular changes

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2
Q

what are the functions that the nervous system manages?

A

structures such as muscles, glands, and organs; heart rate; blood flow; breathing; digestion; urination; and defecation

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3
Q

cranial nerves that carry only sensory fibers

A

I, II, and VIII

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4
Q

cranial nerves that carry only motor fibers

A

III, IV, VI, XI, and XII

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5
Q

cranial nerves that carry both sensory and nerve fibers

A

V, VII, IX, and X

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6
Q

facilitates volunatry motor activity and plays a role in personality traits

A

frontal lobe

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7
Q

receives and interprets sensory input, with the exception of smell, hearing, and vision stimuli

A

parietal lobe

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8
Q

processes visual information

A

occipital lobe

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9
Q

plays an essential role in hearing and memory

A

temporal lobe

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10
Q

includes the thalamus and hypothalamus

A

diencephalon

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11
Q

receives and relays most of the sensory input such as those of pain, termperature, and pressure; affects mood; and initiates body movments

A

thalamus

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12
Q

most inferior portion of the diencephalon; regulates many bodily functions such as temperature, respiratoins, and heart beat. directs hormone secretions of the pituitary

A

hypothalamus

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13
Q

crucial for many basic body functions such as maintaining heart rate, blood pressure, and respirations. collaborates with hypothalamus to regulate these vital activities. injury can easily result in death. origin of many cranial nerves. reflex center for movements of eyeballs, head, and trunk. plays a role in consciousness.

A

brain stem

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14
Q

part of the brainstem that contains nerves that regulate sleep and breathing

A

pons

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15
Q

smallest region of the brainstem, and brain in general. acts as a sort of relay station for auditory and visual information and controls the visual and auditory systems as well as eye movement

A

midbrain

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16
Q

part of the brainstem that is a conduction pathway for ascending and descending nerve tracts. coordinates heart rate, peripheral vascular resistance, breathing, swallowing, vomitine, coughing, and sneezing

A

medulla

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17
Q

acts like a gatekeeper, receiving all incoming and outgoing information. sends impulses to the cerebral cortex through specialized nerve fibers called reticular activation system

A

reticular formation

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18
Q

responsible for alertness during the day and can prevent sleeping at night

A

reticular formation and reticular activation system

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19
Q

communicates with other regions of the brain to coordinate the synergistic motion of muscle movement and balance as well as cognition. coordinates subconscious movements of skeletal muscles. contributes to muscle tone, posture, balance, and equilibrium

A

cerebellum

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20
Q

play a pivotal role in coordination, motor movement, and posture. slow, sustained movments. suppresses useless patterns of movement.

A

basal ganglia

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21
Q

works in conjunction with the hypothalamus to influence instinctive behavior, emotions, motivation, mood, pain, and pleasure

A

limbic system

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22
Q

large opening in the skull through which the spinal cord exits

A

foramen magnum

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23
Q

where does the spinal cord terminate

A

second lumbar vertebrae. here it splits into the cauda equana

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24
Q

how many pairs of spinal nerves are there?

A

31

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25
Q

permits sensation of light touch, pressure, tickling, and itching

A

anterior spinothalamic tracts

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26
Q

allow the sensatoins of pain and temperature

A

lateral spinothalamic tracts

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27
Q

establish the body’s position in relation to the cerebellum

A

spinocerebellar tracts

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28
Q

coordinate movements, especially in the hands

A

corticospinal tracts

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29
Q

responsible for involuntary movements

A

vestibulospinal tracts and reticulospinal tracts

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30
Q

withdrawal reflex that occurs in response to touching an unpleasant stimulus

A

flexor reflex

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31
Q

of the 31 spinal nerves, how many are cervical, thoracic, lumbar, sacral, coccygeal?

A

8 cervical, 12 thoracic, 5 lumbar, 5 sacral, 1 coccygeal

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32
Q

spinal nerves arise from approximately 6-8 small nerves called

A

rootlets

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33
Q

what does each spinal nerve, with the exception of C1 have in common?

A

they each have a specific body surface area from which they obtain sensory information

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34
Q

what are the four plexuses and where are they located?

A

cervical - located from C1 to C4
brachial - from C5 to T1
lumbar - from L1 to L4
sacral - from L4-S4

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35
Q

controls smooth muscles and is responsible for the fight-or-flight response

A

autonomic nervous system

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36
Q

is the autonomic nervous system under conscious control?

A

no

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37
Q

what things does the ANS affect?

A

heart rate, blood pressure, and intestinal motility

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38
Q

what are the two divisions of the ANS?

A

the sympathetic nervous system (SNS) and the parasympathetic nervous system

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39
Q

responsible for fight-or-flight response; initiated when a person is startled or faced with danger and is augmented by secretions from the adrenal medulla

A

SNS

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40
Q

responsible for the rest and digest response

A

parasympathetic nervous system

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41
Q

how will the ANS initiate physiologic responses?

A

by stimulating or inhibiting neurotransmitters and receptors

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42
Q

which receptors does the SNS stimulate and which does the parasympathetic nervous system stimulate?

A

SNS stimulates the adrenergic receptors while the parasympathetic nervous system stimulates the cholinergic receptors

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43
Q

cranial nerve I

A

olfactory

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44
Q

CN II

A

optic

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45
Q

CN III

A

occulomotor

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46
Q

CN IV

A

trochlear

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47
Q

CN V

A

trigeminal

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48
Q

CN VI

A

abducens

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49
Q

CN VII

A

facial

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50
Q

CN VIII

A

vestibulocohlear

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51
Q

CN IX

A

glosopharyngeal

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52
Q

CN X

A

vagus

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53
Q

CN XI

A

spinal accessory

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54
Q

CN XII

A

hypoglossal

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55
Q

condition in which excess CSF accumulates within the skull, which dilates the ventricles and compresses the brain and blood vessels

A

hydrocephalus

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56
Q

what occurs during hydrocephalus?

A

the pressure from the excess CSF thins the cortex, causing severe brain damage.

57
Q

when does CSF accumulate?

A

when the flow is disrupted (referred to as noncommunicating or an obstructive hydrocephalus) or when too much CSF is made or not properly absorbed by the blood stream (referred to as communicating hydrocephalus)

58
Q

is hydrocephalus a common condition?

A

yes

59
Q

when does hydrocephalus occur?

A

it may be present at birth or develop later in life

60
Q

what are risk factors for the development of hydrocephalus at any age?

A

prematurity, pregnancy complications, other congenital defects especially nervous system defects such as spina bifida, nervous system tumors, CNS infections, cerebral hemorrhage, and severe head injuries

61
Q

what do clinical manifestations of hydrocephalus vary depending on?

A

the age group, underlying etiology and disease progression

62
Q

what are the clinical manifestations of hydrocephalus in infants?

A

an unusually large head, a rapid increase in the head size, a bulging fontanelle or soft spot on top of the head, vomiting which is often projectile, lethargy, irritability, high-pitched cry, feeding difficulties, seizures, eyes that gaze downward, developmental delays

63
Q

what are the clinical manifestations of hydrocephalus in older children and adults?

A

headache followed by vomiting, nausea, blurred vision or diplopia, sluggish pupil response to light, eyes that gaze downward, problems with balance, coordination or gait, extreme fatigue, slowing or regression of development, memory loss, confusion, urinary incontinence, irritability, personaility, memory or cognition changes, impaired performance in school or work

64
Q

when does the neural tube usually close?

A

by the fourth week of gestation

65
Q

what occurs with spina bifida?

A

the posterior spinous processes on the vertebrae fail to fuse and this opening permits the meninges and spinal cord to herniate, resulting in neurologic impairment

66
Q

what is the most common site of spina bifida?

A

the lumbar area of the vertebrae

67
Q

what is the cause of spina bifida?

A

the exact cause is unknown but it is thought to be a result of genetic and environmental influences

68
Q

who is spina bifida most common in?

A

caucasians and hispanics

69
Q

what are maternal risk factors for the development of spina bifida?

A

family history of neural defects, folate deficiency, certain medications, diabetes mellitus, prepregnancy obesity, and increased body temperature (from fevers, hot tubs, saunas, and tanning beds)

70
Q

what complications can arise because of spina bifida?

A

physical and neurologic impairments as well as hydrocephalus and meningitis

71
Q

do children with spina bifida usually have deficits in intelligence?

A

no they are usually of normal intelligence but may have learning problems because of the chronic nature of the condition

72
Q

mildest and most common form of spina bifida. results from a small gap in one or more of the vertebrae. the spinal nerves and meninges do not usually protrude through the opening so children with this usually do not have any manifestations and experience no neurological deficits

A

spina bifida occulta

73
Q

what may be a sign of spina bifida occulta?

A

the child may have a dimple, birthmark, or tuft of hair over the site

74
Q

rare form of spina bifida where the meninges and CSF protrude through the vertebral opening and form a sac on the surface of the infants back. there is no nerve tissue in the sac.

A

meningocele

75
Q

is neurologic impairment common with meningocele?

A

no, it is usually not present and these membranes can be removed by surgery with little or no damage to nerve pathways. neurologic impairment can develop if there is infection or rupture of the sac.

76
Q

most severe form of spina bifida. the spinal canal remains open along several vertebrae in the lower and middle back and the meninges, spinal cord, spinal nerves, and CSF protrude through this large opening to form a sac on the infants back

A

myelomeningocele

77
Q

why is the infant so vulnerable to life-threatening infections when they have myelomeningocele?

A

because the tissues and nerves are exposed if the sac is not covered by skin

78
Q

what are some complications that can arise with myelomeningocele?

A

neurologic impairment, bowel and bladder problems, seizures

79
Q

group of non-progressive disorders that appear in infancy or early childhood and permanently affect motor movement, muscle coordination, and other cerebral functioning

A

cerebral palsy (CP)

80
Q

when does CP usually develop?

A

damage to the cerebellum during the prenatal period, but it can occur any time during the first three years of life when the brain is developing

81
Q

is CP curable?

A

no, but the right treatment can make an impact on the child’s prognosis

82
Q

what are factors that contribute to the development of CP?

A

prematurity, breech births, multiple fetuses, hypoxia, hypoglycemia, cerebral hemorrhage, neurologic infections, head injury, maternal infection during pregnancy, maternal exposure of toxins during pregnancy, severe jaundice

83
Q

what is CP classified based on? what are the three classifications?

A

based upon the movement disorder involved, which reflects the area of the brain affected. spasticity (stiff muscles, most common), dyskinesia (uncontrolled movement), ataxia (poor balance and coordination)

84
Q

what parts of the body might CP affect?

A

may affect the entire body or just one area, may affect one side or both sides of the body

85
Q

what are clinical manifestations of CP?

A

persistence of early reflexes, developmental delays, ataxia, spasticity, flaccidity, hyperreflexia, asymmetrical walking gait with one foot or leg dragging, unusual positioning of limbs when resting or when held up, excessive drooling, difficulties swallowing, sucking, or speaking, facial grimaces, tremors, difficulty with precise motion

86
Q

what are complications that can develop because of CP?

A

balance and coordination issues, contractures, scoliosis, malnutrition, communication issues, learning or cognitive difficulties, seizures, vision and hearing loss, urinary incontinence, constipation, osteoporosis, chronic pain, injury

87
Q

an inflammation of the meninges, usually resulting from an infection. the CSF may also become affected.

A

meningitis

88
Q

what things can cause meningitis?

A

any number of bacterial or viral agents, chemical irritants, tumors, fungi, parasites, and allergens

89
Q

how do the infectious agents invade the meninges in meningitis?

A

through the blood or nearby structures, or through direct access

90
Q

what are risk factors for the development of meningitis?

A

being younger than 25, living in a community setting, pregnancy, working with animals, and immunodeficiency

91
Q

is meningitis life-threatening?

A

it can be self limiting or life threatening

92
Q

what are some complications that can occur because of meningitis?

A

permanent neurologic damage, seizures, hearing loss, blindness, speech difficulties, learning disabilities, behavior problems, paralysis, acute renal failure, adrenal gland failure, cerebral edema, shock, and death

93
Q

what are the clinical manifestations of meningitis?

A

initially mimic influenza infections. fever and chills, mental status changes, nausea and vomiting, photobia, severe headache, stiff neck, agitation, bulging fontanelle, decreased consciousness, opisthotonos, poor feeding or irritability in children, tachypnea, tachycardia, rash

94
Q

when the brain collides with the skull or any penetrating object this is called

A

a traumatic brain injury

95
Q

what things usually cause a TBI

A

a sudden and violent blow or jolt to the head, penetrating head wound that disrupts the brains normal function

96
Q

what are the main sources of TBIs?

A

falls, motor vehicle accidents, penetration of an object, and assaults

97
Q

what people are at higher risk for experiencing a TBI?

A

males are twice as likely as females, young children and 15-19 year olds, adults 75+, certain military personnel, African Americans

98
Q

many TBIs will result in a wide range of long-term and potentially life-altering complications such as…

A

changes in thinking, sensation, language or emotions

99
Q

what can TBIs increase the risk for?

A

seizures, migraine headaches, Alzheimer’s disease, and Parkinson’s disease

100
Q

true or false: neurologic dysfunction will not result from multiple small TBIs

A

false, multiple mild TBIs can have an accumulative effect and result in neurologic dysfunction, cognitive deficits, and death

101
Q

momentary interruption in brain function that usually results from a mild blow to the head that causes sudden movement of the brain, disrupting neurologic function

A

concussion

102
Q

what things may follow a concussion for weeks or months?

A

amnesia, confusion, sleep disturbances, and headaches

103
Q

bruising of the brain accompanied by rupture of small blood vessels and edema

A

cerebral contussion

104
Q

what do most contussions result from?

A

a blunt blow to the head that causes the brain to make sudden impact with the skull

105
Q

the initial area where the brain impacts the skull

A

coup

106
Q

the area where the brain impacts the opposite side of the skull after it has rebounded

A

countercoup

107
Q

type of fracture located at the base of the skull and is usually accompanied by CSF leakage

A

basilar skull fracture

108
Q

how may clinical manifestations of a TBI develop?

A

they may develop slowly or they may be sudden and severe. symptoms may improve and then suddenly worsen

109
Q

what should the individual be asked when a TBI is suspected?

A

to give an account of the accident. not being able to recall details is an indication of a TBI

110
Q

what are clinical manifestations of TBIs?

A

indications of a concussion, changes in or unequal size of pupils, seizures, asymmetrical facial features, fluid drainage from the nose, mouth, and ears, fracture in the skull or face, bruising of the face, swelling at the site of injury, scalp wound, impaired senses and speech, inability to move one or more limbs, irritability, personality changes, or unusual behavior, loss of consciousness, bradypnea, hyptension, restlessness, lack of coordination, lethargy, stiff neck, vomiting

111
Q

increased volume in the limited space of the cranial cavity

A

increased intracranial pressure

112
Q

what is the Monro-Kellie hypothesis

A

hypothesis that states that the cranial cavity cannot be compressed, and that the volume inside the cavity is fixed. the skull and its components create a state of volume equilibrium, such that any incres in the volume of one component must be compensated by a decrease in the volume of another component

113
Q

how does the brain usually compensate for increased ICP?

A

by shifts in the CSF and to a lesser extent, blood volume. these fluids respond to increases in the volume of remaining components

114
Q

what do transient increases in ICP routinely occur with?

A

position changes, coughing, or sneezing

115
Q

what are two compensatory mechanisms to maintain tissue perfusion?

A

autoregulation and Cushing’s syndrome

116
Q

when the blood vessels dilate to increase blod flow and constrict if the ICP is increased

A

autoregulation

117
Q

complex cascade of events that results in increased blood pressure. when the mean arterial pressure drops below the ICP, the hypothalamus increases sympathetic stimulation causing vasoconstriction, increased cardiac contractility, and increased cardiac output

A

Cushing’s reflex

118
Q

if unresolved, increased ICP leads to a trio of effects known as

A

Cushing’s triad - increased blood pressure, bradycardia, and changes in respiratory pattern

119
Q

what causes bradycardia with increased ICP?

A

it can be caused because the baroreceptors in the carotid arteries detect the increase in blood pressure and trigger the parasympathetic response through vagal stimulation or it could be because the increased ICP impinges on the vagal nerve, causing a parasympathetic response

120
Q

as pressure increases inside the skull and space becomes limited, what happens?

A

brain tissue shifts downward

121
Q

what respiratory changes usually occur with increased ICP on the brainstem

A

Cheyne-Stokes respirations and bradypnea

122
Q

what are the clinical manifestations of increased ICP?

A

decreasing level of consciousness, vomiting which is often projectile, increasing blood pressure with increasing pulse pressure, bradycardia, papilledema, fixed and dilated pupils, posturing, behavior changes, severe headache, lethargy, neurologic deficits, seizures. two manifestations unique to infants are separated sutures and bulging fontanelles

123
Q

flexion of the arms, wrists, and fingers with adduction in upper extremities, extension, internal rotation, and flantar flexion in lower extremities

A

decorticate response

124
Q

all four extremities in rigid extension with hyperpronation of forearms and plantar extension of the feet

A

decerbate response

125
Q

left side of the body and decerebrate response on the right side of the body

A

decorticate response

126
Q

collection of blood in the tissues that develops from ruptured blood vessels

A

hematoma

127
Q

result from bleeding between the dura and skull, usually caused by an arterial tear

A

epidural hematoma

128
Q

what are the clinical manifestations of a hematoma?

A

marked neurologic dysfunction that usually develops within a few hours of injury. brief loss of consciousness, followed by a short period of alertness, then loss of consciousness again

129
Q

hematoma that develops between dura and the arachnoid and are frequently caused by a small venous tear

A

subdural hematomas

130
Q

type of subdural hematoma in which manifestations of neurologic deficits are present within 24 hours of injury. this type progresses rapidly and has a high mortality. ICP increases over a period of about a week after the injury

A

acute subdural hematoma

131
Q

type of subdural hematoma in which the manifestations develop several weeks after an injury because of a slow leak. more common in elderly adults because of the brain atrophy that occurs with age, which give the hematoma more space to develop

A

chronic subdural hematoma

132
Q

result from bleeding in the brain tissue itself. usually caused by contusion or shearing injuries, but can also result from hypertension, cerebral vascular acidents, aneurysms, or vascular abnormalities

A

intracerebral hematomas

133
Q

results from bleeding in the space between the arachnoid and pia. its primary clinical presentation is a severe headache that has a sudden onset and is worse near the back of the head

A

subarachnoid hemorrhage

134
Q

in all types of hematomas, what does the bleeding lead to?

A

localized pressure on nearby tissue and increases intracranial pressure

135
Q

how can a hematoma increase ICP?

A

the hematoma becomes encapsulated by fibroblasts and blood cells within the capsule lyse. the fluid from the hemolysis exerts osmotic pressure drawing more fluid into the capsule. the edema increases the size of the mass, applying pressure on surrounding tissue and increasing ICP. bleeding can trigger vasospasms, worsening ischemia.

136
Q

result from direct injury to the spinal cord or indirectly from damage to surrounding bones, tissues, or blood vessels

A

spinal cord injuries

137
Q

what are the main causes of spinal cord injuries?

A

falls, motor vehicle accidents, violence, ans sports injuries. mild injuries can occur because of weakening of vertebral structures. direct damage can occur if the spinal cord is pulled, pressed sideways, or compressed

138
Q

temporary suppression of neurologic function because of spinal cord compression. neurologic function gradually returns.

A

spinal shock

139
Q

who is spinal cord injuries most common in?

A

caucasians and males between the ages of 15 and 35 years

Pathophysiology (11 decks)

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