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Pathophysiology > Neurological system > Flashcards

Neurological system Flashcards

1
Q

what percentage of CO does the brain recieve

A

15-20%

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2
Q

what are the 3 components of the brain

A
  • forebrain
  • midbrain
  • hindbrain
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3
Q

what comprises the brain stem

A

midbrain, medulla and pons

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4
Q

reticular formation

A

the collection of nerve cell bodies within the the brainstem that connect the brainstem to the cortex that control the vital reflexes

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5
Q

spinal cord

A

lies within the vertebral column

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6
Q

upper motor neurons

A
  • completely contained within the CNS
  • control fine motor movement influences spinal reflex arcs
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7
Q

lower motor neurons

A
  • project into periphery
  • directly influence muscles
  • cell body is in the grey matter of the spinal column and brainstem , but extend to the PNS
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8
Q

damage to the upper neurons results in

A

intital paralysis followed by partial recovery

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9
Q

damage to the lower neurons results in

A

paralysis unless peripheral nerve damage is followed by nerve regeneration

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10
Q

frontal lobe functions

A
  • problem solving
  • emotional traits
  • reasoning
  • speaking
  • voluntary motor activity
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11
Q

temporal lobe function

A
  • understanding language
  • behaviour
  • memory
  • hearing
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12
Q

brain stem functions

A
  • breathing
  • body tempurature
  • digestion
  • alertness/sleep
  • swallowing
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13
Q

cerebellum functions

A
  • balance
  • coordination and control of voluntary movements
  • fine muscle control
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14
Q

occipital lobe function

A
  • vision
  • color perception
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15
Q

parietal lobe function

A
  • knowing right from left
  • sensation
  • reading
  • body orientation
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16
Q

what are the 3 components of the neuron

A

cell body
dendrites
axon

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17
Q

dendrites

A

carry nerve impulses towards the cell body

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18
Q

axon

A

carry nerve impulses away from the cell body

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19
Q

myelin sheath

A
  • wraps around the axon
  • speeds up impulse propagation
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20
Q

schwann cells

A

form myelin sheath around axon

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21
Q

which injuries will heal faster: crushing or cut injuries

A

crush

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22
Q

effect of scaring on nerve regeneration

A

block or slow

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23
Q

cranium

A

protects brain and associated structures

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24
Q

meninges

A
  • 3 protective membranes
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25
Q

subarachoid space

A
  • lies between the arachnoid and pia layers
  • contains cerebrospinal fluid
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26
Q

cerebralspinal fluid

A
  • intercranial and spinal structures float in the CSF
  • protect from injury
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27
Q

____ ml of CSF is circulating in the subarachnoid space and ventricles

A

150 ml

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28
Q

___ml of CSF produced daily

A

600

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29
Q

where is CSF formed

A

in the ventricles

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30
Q

how many cervical vertebrae are there

A

8

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31
Q

how many thoracic vertebrae are there

A

12

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32
Q

how many lumbar vertebrae are there

A

5

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33
Q

how many sacral vertebrae are there

A

5

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34
Q

how many coccygeal vertebrae are there

A

1

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35
Q

what is the primary regulator for blood flow in the CNS

A

carbon dioxide

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36
Q

carbon dioxide

A
  • primary regulator for blood flow in the CNS
  • potent vasodialator
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37
Q

circle of Willis

A
  • provides an alternative route for collateral blood flow if one of the contributing arteries is occluded
  • saftey valve for the brain
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38
Q

blood brain barrier

A
  • cellular structures that selectively inhibit potentially harmful substance from entering the interstitial spaces of the brain or CSF
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39
Q

what kind of alterations are there

A
  • structural
  • metabolic
  • psychogenic
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40
Q

structural alterations

A
  • infection, vascular alterations, neoplasms, traumatic injury, congenital degenerative and polygenic traits, and metabolic disorders
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41
Q

metabolic alterations

A
  • alterations in the delivery of energy
  • hypoxia, electrolyte disturbances, or hypoglycemia, disorders causes by renal or liver
  • alter neuron excitability as medications and toxins are not properly cleared
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42
Q

psychogenic alterations

A
  • psychiatric disorders
  • appear unconciousness but are actually awake
  • unrespnsiveness
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43
Q

level of conciousness is tested with

A

glasgow coma scale

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44
Q

if LOC decreases the brain relies on _____ to regulate respiration

A

carbon dioxide levels

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45
Q

confusion

A

loss of ability to think rapidly and clearly; impaired judgement and decision making

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46
Q

disorientation

A

the person may exhibit restlessness, anxiety, and irritation; disorientation to time occurs followed by disorientation to place and familar others and impaired memory; recognition of self is lost last

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47
Q

lethargy

A
  • limited spontaneous movement or speech; easy arousal with normal speech or touch; orientation to time, place, or person may or may not occur
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48
Q

obtundation

A
  • mild to moderate reduction in arousal (awakeness) with limited response to enviorment; falls asleep unless stimulated verbally or tactiley; answers questions with minimal response
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49
Q

stupor

A
  • condition of deep sleep or unresponsiveness from which person may be aroused or caused to open eyes only by vigorous and repeated stimulation; response is often withdrawn or grabbing at stimulus
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50
Q

coma

A
  • associated with nonpurposeful movement only on stimulation
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51
Q

pupillary changes

A
  • indicate level of brainstem dysfunction
  • brainstem control of arousal is adjacent to area that control pupils
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52
Q

oculomotor responses

A
  • resting spontaneous, and reflexive eye movements change with the level of consciousness of the patient
  • medications should not change reflexes but destructive or compression injuries to the brainstem will cause specific abnormalities
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53
Q

dysconjugate movement

A

indication of brain injury

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54
Q

motor responses classifications

A
  • purposeful
  • inappropriate or not present
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55
Q

how to test motor responses

A

ask patient to squeeze finger

56
Q

decorticate flexion

A
  • bringing into the core
  • assoicated with hemisphere damage above the midbrain
57
Q

decerebrate posturing

A
  • associated with severe damage involving the midbrain and upper pons
58
Q

normal sized pupils

A

2-5mm

59
Q

aneurysm

A

dilated pupils

60
Q

cluster headache effect on the pupils

A

constricted pupils

61
Q

glaucoma efffect on the pupils

A

mid dilated pupils

62
Q

head trauma effect on the pupils

A

unequal sized pupils

63
Q

syphilis effect on the pupils

A

small pupils that. constrict poorly to direct light

64
Q

selective attention

A
  • ability to focus
  • choose what we are going to pay attention to
65
Q

selective attention deficits may be caused by

A

seizures, contusions, subdural hematomias, stroke, neoplasms, alzheimers disease, dementia

66
Q

memory

A

recording, retention, and retrial of information

67
Q

amnesia

A

mild or severe is loss of memory

68
Q

retrograde amnesia

A
  • difficultly with past personal history or facts
69
Q

anterograde amnesia

A

inability to form new memories

70
Q

executive attention deficits

A
  • inability to maintain sustained attention and working memeory deficit
71
Q

ADHD

A
  • ability to function is impaired by inattentiveness, hyperactivity impulsivity
72
Q

agnosia

A

failure to recognize the form and nature of objects

73
Q

agnosia types

A
  • tactile
  • visual
  • auditory
74
Q

agnosia is assoicated with

A

damage caused by cerebral accidents which cause damage to specific areas of the brain

75
Q

dysphasia

A

impaired comprehension or production of language

76
Q

aphasia

A
  • most severe form of dysphasia
  • inability to communicate using language
77
Q

dysphasia in the brocas area

A
  • cant create speach
78
Q

dysphasia in the wernickes are

A

cant comprehend speech

79
Q

aphasia ia caused by

A

injuries and disease
- vascular, neoplastic, traumatic, degenerative, metabolic, or infectious

80
Q

primary injury

A

initial trauma

81
Q

secondary injury

A
  • result of the alteration in the cerebral blood slow, intercranial pressure, and oxygen delivery
  • can occur within seconds or days
82
Q

cerebral perfusion pressure (CPP) formula

A

MAP-ICP

83
Q

increased intercranial pressure is due to

A

increased intercrainial content
- tumours, edema, excess CSF, or hemmorage

84
Q

stage 1 of compensation

A
  • brain is trying to compensate mainly through vasoconstricition
  • patient may be asymptomatic
85
Q

stage 2 of compensation

A
  • intercranial pressure is increasing beyond the brains ability to compensate
  • cellular hypoxia worsens
  • body attempts to compensate through vasoconstriction
  • patient will show signs of increased intercrainal pressure
86
Q

sings of decreased level of conciousness

A
  • widening pulse pressure, decreased heart rate, pupils small and sluggisn
87
Q

signs of increased intercrainial pressure

A

confusion, restlessness, decreased level of conciousness

88
Q

stage 3 of compensation

A
  • inter cranial pressure is approaching arterial pressure
  • cellular hypoxia worsens; patient becomes hypercapnia
  • patient will decompensated quickly
  • intervention is required quickly
  • decreased level of consciousness, widened pulse pressure, decreased heart rate, pupils small and sluggish
89
Q

stage 4 of compensation

A
  • brain in herniating
  • intercranial pressure equals arterial pressure which prevents cerebral perfusion, hypoxia lead to cellular dealth which will further increase ICP
  • patient is past the point of receovery
  • ‘blown pupils”
  • HR, BP, will decreased
  • cheyne-stoke breathing
90
Q

cushing triad

A
  • occurs in the late stages of acute head injury
  • indicates brain stem herniation is imminent
  • increased BP, decreased Pulse rate, irregular breathing rate
91
Q

cerebral edema

A
  • type of dependent edema
  • increase in the fluid content of the brain tissue
92
Q

cerebral edema causes

A
  • distortion of blood vessels, displacement of brain tissues, increase in ICP, and eventually herniation
93
Q

cytotoxic or metabolic edema

A
  • early stages; blood brain barrier stays intact
  • failure of the active transport systems (cell lose potassium and gain sodium (water follows))
94
Q

cytotoxic or metabolic edema is treated with

A

diuretics

95
Q

interstitial edema

A
  • caused by blockage of CSF pathways
96
Q

vasogenic edema

A
  • late stages
  • blood brain barrier compromised
97
Q

vasogenic edema is caused by

A

increased permeability of the capillary endothelium of the brain
- injury of the vascular structures

98
Q

vasogenic edema process

A

plasma proteins leak into the extracellular spaces, drae water to then; start in area of injury and spreads to white matter of the same side; edema promotes moe edema and ischemia

99
Q

signs and symptoms for cerebral edema

A
  • headache, stiffness, nausea and vomiting, vision loss, memory loss, loss of muscle coordination
100
Q

hypotonia

A
  • decreased muscle tone
  • passive movement of a muscle
  • has little resistance if any
101
Q

hypotonia is caused by

A
  • cerebral damage (causing ataxia and tremor)
  • pained with exaggerated reflexes
    ‘- spinal cord injury or cerebral vascular accident where nerve impulses are lost
102
Q

hypotonia sings and symptoms

A

weak and tire easily, difficulty rising from seating, walking up the stairs, joints become hyperflexible, loss of muscle tone (look flabby and flat)

103
Q

hypertonia

A
  • increased muscle tone
  • passice muscle movement with resistance to stretch
104
Q

hypertonia is caused by

A
  • upper neuron damage
  • spasticity, paratonia, dystonia or rigidity
105
Q

paratonia

A

inability to relax muscle during assesment

106
Q

dystonia

A

contract uncontrollably

107
Q

hypertonia signs and symptoms

A
  • tire easily, weakness
  • passive and active affected equally, can see either hypotrophy or hypertrophy dependent on decrease in muscle use or overstimulation of muscle fibres
108
Q

hyperkinesia

A
  • excessice purposeless movements
  • could be tremors, or abnormal involuntary movements
109
Q

dyskinesia

A
  • abnormal movements that occur as spasms
  • tardice dyskinesia is movements of the face
110
Q

dyskinesia example

A

tourettes syndrome

111
Q

hypokinesia

A
  • loss of involuntary movement
  • decrease of slowness in voluntary movements
  • delay in time it takes to start to preform a movement
112
Q

spinal shock

A
  • temporary loss of all spinal cord function below the level of the lesion
  • consequence of spinal cord injury
  • destruction of efferent pathways) sending message down)
113
Q

spinal shock initial symptoms

A
  • complete paralysis, absence of reflexes, motor, sensory, autonomic function, including disturbances in bowel and bladder function
  • can last hours
114
Q

paresis

A

condition of muscle weakness caused by nerve damage or disease

115
Q

paralysis

A
  • loss of muscle function in part of your body
116
Q

hemiparesis/hemiplegia

A
  • one side
    EXAMPLE: stroke
117
Q

diplegia

A
  • injuries of specific part of the brain
118
Q

paraplegia

A
  • lower extremities due to spinal cord injury
119
Q

quadriplegia

A
  • all four extremities due to spinal cord injury
120
Q

brain death

A
  • brain damage is beyond the point of recovery
  • brainstem fucntions have stopped
  • not reversible
121
Q

brain death example

A

drug overdose

122
Q

test to confirm brain death

A

dolls eyes, corneal reflex, ice in ears

123
Q

cerebral dealth or irreversible coma

A
  • dealth of the hemispheres - damage is permanent
  • brain stem continues to maintain homeostasis
  • person does not speak, open their eyes or have purposeful mevements, these individuals will not recover
  • not candidates for organ donation
124
Q

vegetative state

A
  • unawareness of self or surrounding enviorment
  • does not speak or understand speech, cannot follow commands, sleep-wake cycles present, spontaneous eye opening, BP and resps
125
Q

a vegatative state lasts longer than __ _____ are considered permanent

A

12 months

126
Q

locked-in syndrome

A
  • complete paralysis of voluntary muscles (except eyes)
  • fully conscious but unable to communicate except through eye movements
127
Q

astrocytoma

A
  • most common brain tumour across the lifespan (30-50%)
128
Q

astrocytoma grade 1 and 2

A

slow growing

129
Q

astrocytomas grade ____ are more common in children and younger people

A

1-3

130
Q

grade 4 astrocytoma

A
  • called glioblastoma
  • most common type of lethal astrocytoma
131
Q

extracerebral neoplasma

A

growth in the meninges outside the cerebrum
- usually originate from the meningeal cells in the dura mater
- slow growing

132
Q

nerve sheath tumours

A
  • autosomal dominant, disorder produces neurofibromas
  • can occur peripherally (type1); or centrally (type 2)
  • slow growing
  • usually benign
133
Q

nerve shealth signs and symptoms

A

muscle weakness, numbness, tingling

134
Q

metastatic

A
  • secondary tumours
135
Q

primary sites for metastatic tumours

A

lung, breast, kidney, colon and skin

136
Q

signs and symptoms of brain tumours

A
  • diminished cognitive functioning (behavioural alteration), headache, vomiting, seizures, papilledema, unsteady gait, loss of sphincter control
137
Q

metastatic brain tumors signs and symptoms

A
  • headache, nervousness, depression, trembeling, confusion, forgetfulness, and gait disorders

Pathophysiology (22 decks)

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