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Pathophysiology > Chapter 16 - Disorders Of CNS, PNS, NMJ > Flashcards

Chapter 16 - Disorders Of CNS, PNS, NMJ Flashcards

1
Q

Alterations of CNS function

A

Involve traumatic injury, vascular disorders, tumour growth, infections and inflammatory processes

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2
Q

Alterations of PNS function

A

Involve nerve route, nerve plexus, nerves themselves or neuromuscular junction

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3
Q

Primary cause of death and disability in individuals under age of 40

A

traumatic brain injury

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4
Q

What is the percentage of TBIs sustained by children and youth and why?

A

30%
-usually sports and recreational activities

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5
Q

TBI

A

Alteration in brain function or other evidence of brain disease caused by an external force

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6
Q

Primary TBI

A

Direct impact
-focal or diffuse

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7
Q

what is focal and diffuse, and what are the percentages of

A

Focal- affecting one area 2/3

Diffuse- involving more than one, atonal injury 1/3

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8
Q

Secondary TBI

A

Indirect result of primary injury
-systemic responses and cascade of cellular/molecular cerebral events

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9
Q

TBI diagnosis

A

Glasgow coma scale (GCS)

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10
Q

Score 2

A

Eye opening to pain, incomprehensible sounds, extension to pain

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11
Q

Score 3

A

Eye opening to verbal command, inappropriate words, flexion to pain

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12
Q

The lower the score the

A

More severe the damage

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13
Q

Primary focal

A

Can be closed or open injury

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14
Q

Closed primary focal

A

More common
-head striking hard surface, moving object striking head or blast waves
-dura mater remains intact, brain tissue not exposed

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15
Q

Open primary focal

A

Penetrating trauma or skull fracture
-break in dura mater, brain tissue is exposed

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16
Q

Severe cases of primary focal closed brain injury

A

Contusions, epidural, subdural, hematomas

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17
Q

Mild primary focal closed BI

A

80 percent of cases

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18
Q

Coup or contrecoup

A

Coup= injury at site of impact
Countrecoup= injury from brain bouncing back and hitting opposite side of skull

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19
Q

Contusions

A

Compression of skull at point of impact produces a contusion
-blood leaking from injured vessel

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20
Q

Smaller contact area =

A

More severe the injury

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21
Q

Edema forms which increases ICP =

A

Hemorrhages, edema, infarction, necrosis and tissue becomes pulpy

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22
Q

Most common site of contusions

A

Frontal lobe

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23
Q

Greatest injury effects how many hours after injury

A

18-36 hours

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24
Q

Diagnosis for contusions

A

Glasgow coma scale, CT scan or MRI

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25
Q

TX for contusions

A

Surgical removal of large contusions and areas of hemorrhage may be required

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26
Q

Epidural

A

Skull fracture, hemiparesis, pupil dilation, loss of consciousness

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27
Q

Subdural

A

Fast/hemianopia or alcohol, craniotomy, membrane forms around hematoma

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28
Q

Intracerebral

A

Frontal temporal, penetrating steering, pupil dilation, positive babinksi

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29
Q

Epidural hematomas

A

Bleeding between dura mater and skull
-artery bleeding, hematoma

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30
Q

Most common site of epidural hematomas

A

Temporal fossa

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31
Q

Most common site of epidural hematomas

A

Temporal dosas

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32
Q

Symptoms and epidural hematomas

A

-lose consciousness
-as it grows, more headache, confusion, seizure
-hemiparesis
-pupil dilation

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33
Q

Hemiparesis

A

Weakness or inability to move one side of body

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34
Q

Pupil dilation and prognosis

A

Injury prognosis is good if treated before both pupils dilate

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35
Q

TX for epidural hematomas

A

Medical emergency

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36
Q

Subdural hematomas

A

Bleeding between dura mater and brain

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37
Q

Acute subdural hematomas

A

Develop quickly, within hours
-as it grows, ICP rises and pressure is applied to veins assisting in short term limitation

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38
Q

Symptoms for acute subdural hematomas

A

Headache/confusion
-hemianopia
-anopia

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39
Q

Hemianopia

A

Blindness over half of vision field

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40
Q

Anopia

A

Blindness

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41
Q

Chronic subdural hematomas

A

Develop over weeks to months
-common in alcohol abuse
-mass bleeding, subdural space fills with blood
-formation of vascular membrane around hematoma

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42
Q

Symptoms of chronic subdural hematomas

A

Headaches, tenderness over hematoma
-worsening dementia, paratonia (rigidity)

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43
Q

TX for chronic subdural hematomas

A

Craniotomy to remove jelly like blood

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44
Q

Intracerebral hematomas

A

Bleeding within the brain
-2 to 3 percent of head injuries
-frontal and temporal lobe

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45
Q

Intracerebral hematomas: penetrating and shearing forces injure small blood vessels =

A

Growing mass/edema

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46
Q

Symptoms of Intracerebral hematomas

A

Sudden rapid decrease in level of consciousness
-pupil dilation, positive babinski reflex

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47
Q

Positive babinski reflex

A

When big toe bends up and back of food and other toes fan out

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48
Q

Examples of primary focal closed

A

-coup/contrecoup
-contusion
-epidural hematoma
-subdural hematoma
-Intracerebral hematoma

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49
Q

Primary focal open

A

Compound skull fracture/ missile injuries

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50
Q

Primary diffuse injury

A

Diffuse brain injury

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51
Q

Open brain injury

A

Trauma penetrates dura mater and creates both focal and diffuse injury
-compound skull fractures and misleading injuries

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52
Q

Compound skull fracture

A

Opens a path between cranial contents and environment
-whenever cuts of the scalp, tympanic membrane, sinuses, eye or mucous membranes occur a CSF should be considered

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53
Q

Cause of CSF are crush or stretch injury

A

Crush: includes cutting or crushing - whatever missile touches

Stretch: blood vessels and nerve damage - without direct contact

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54
Q

Most open brain injury become

A

Unconscious

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55
Q

Basilian skull fractures

A

Usually caused by substantial blunt force trauma
-at least one of the bones that compose base of skull
-generate spinal fluid leaking from ear to nose = blackened eyes

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56
Q

Diffuse brain injury =

A

Injury widespread in brain

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57
Q

Primary diffuse brain injury

A

Effects from high levels of acceleration and deceleration or rotational forces
-can shear axonal fibres + white matter tracts

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58
Q

Degree of shearing =

A

Cognitive consequences = extensive cognitive impairments

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59
Q

Degree of shearing =

A

Cognitive consequences

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60
Q

Diagnosis of primary diffuse injury

A

Electron microscope to detect axonal damage

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61
Q

Secondary brain injury

A

Indirect result of primary brain injury, including both trauma and stroke syndromes

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62
Q

Systemic

A

Hypotension, hypoxia

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63
Q

cerebral

A

Inflammation, edema, inc ICP

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64
Q

Primary effects cause

A

Disruption to BBB causing neuronal death

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65
Q

Management of secondary brain injury

A

-prevent hypoxia, maintain cerebral perfusion pressure and removal of hematomas
-nutritional management is critical

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66
Q

mild TBI

A

Mild concussion
-immediate transitory clinical manifestations

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67
Q

Mild TBI consciousness

A

Less than 30 min

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68
Q

Glasgow score for mild TBI

A

13-15

69
Q

Symptoms of mild TBI

A

Headache, nausea, vomiting

70
Q

Diagnosis of mild TBI

A

Blood test to determine need for CT scan

71
Q

Moderate TBI

A

Moderate concussion
-permanent defects in arousal and attention

72
Q

Moderate TBI consciousness

A

Lasts more than 30 mins up to 6 hours

73
Q

Glasgow score for a moderate TBI

A

9-12

74
Q

Symptoms of moderate TBI

A

Confusion, amnesia (more than 24 hours), brain imaging is abnormal

75
Q

Severe TBI

A

Severe concussion
-permanent damage to vegetative state to death

76
Q

Consciousness and Glasgow score for a severe TBI

A

More than six hours, 3-8

77
Q

Signs of severe TBI

A

-Change in Pupillary reaction, cardiac and respiratory systems
-decorticate or decerebrate posturing
-inc ICP 4-6 days after injury

78
Q

Symptoms of a severe TBI

A

Compromised coordinated movements, verbal and written communication

79
Q

TX fro severe TBI

A

Maintain cerebral perfusion and promote neural protection

80
Q

Complications of TBI

A

Severity and brain location determine probable complications

81
Q

Post concussion syndrome

A

Lasts weeks to months after concussion
-important to have 24 hours of close observation

82
Q

Post concusssion syndrome symptoms

A

-drowsiness, confusion, vomiting
-unequal pupils
-csf drainage from ears or nose
-double vision

83
Q

Post traumatic seizures

A

Epilepsy
-10 to 20 percent of TBI
Molecular changes = sprouting of new hyperexcitable neural activity = inc seizures

84
Q

Highest risk for post traumatic seizures

A

Open brain injuries

85
Q

Chronic traumatic encephalopathy

A

Progressive deleting disease that develops with repeated brain injury
-contact sports, blast injuries

86
Q

Chronic traumatic encephalopathy consequences

A

Violent behaviour, change in cognitive, motor function, depression, suicide

87
Q

What tangles occur in brain (chronic traumatic encephalopathy

A

Tau neurofibrillary

88
Q

Who are particularly at risk for spinal cord and vertebral injury

A

Males 20-39 yoa, adults 79+ yoa

89
Q

Primary spinal cord injury

A

Injury occurs if an injured spine does not receive adequate immobilization following trauma

90
Q

C1-C4 is

A

Life threatening due to loss of CV and respiratory function

91
Q

Secondary spinal cord injury

A

Disease causing process occurring within minutes and continues for weeks
-hemorrhage in grey matter (death of entire grey matter)

92
Q

Cord swelling =

A

Inc dysfunction = difficult to distinguish permanent and temporary damage

93
Q

Death of oligodendrocytes =

A

Myelin degeneration

94
Q

Vertebral fractures, dislocation, bone fragments =

A

Shearing and compression

95
Q

Vertebrae fracture easily due to

A

Torn supporting ligaments

96
Q

Vertebral injuries occur at the

A

Most moveable portions of column

97
Q

Hyperextension

A

Disruption of intervertebral discs

98
Q

Flexion

A

Vertebral wedge fracture

99
Q

Rotation

A

Shearing force and rupture of ligament support

100
Q

Manifestations of vertebral injuries: spinal shock

A

Immediate development, loss of function at or below level of injury
-hypothalamus cannot regulate body heat, person assumes temperature of air

101
Q

Poikilothermic

A

Person assumes temperature of air

102
Q

Spinal shock lasts, and returns

A

Lasts: 7-20 days

Returns: with reflex emptying of bladder

103
Q

Manifestations of vertebral injuries: neurogenic shock

A

Occurs with injury above T6
-unopposed parasympathetic activity
-results in vasodilation and hypotension

104
Q

Migraine

A

Episodic, genetic, environmental, hyperoccipital (vision)

105
Q

Cluster headaches

A

Many attacks per day, remission, trigeminal nerve

106
Q

Tension headaches

A

Episodic, tight band around head, trigeminal nerve

107
Q

Three classifications of migraines

A
  1. With aura
  2. Without aura
  3. Chronic
108
Q

Occurrence of migraines in Canada (men, women, children)

A

M- 8
W- 25
C-10

109
Q

Aura

A

Beings as spreading neural hyperactivity in occipital brain region
-visual processing regions

110
Q

Premonitory phase

A

Symptoms occur hours to days before onset of aura
-tired, irritable

111
Q

Migraine aura

A

1/3 of persons have aura symptoms that last up to 1 hour

112
Q

Headache phase

A

Begins on one side of head, spreads to entire head

113
Q

Recovery phase

A

Irritability, fatigue

114
Q

Who primarily has cluster headaches

A

Men 20 to 50 yoa

115
Q

Pathophysiology of cluster headaches

A

Pain related to neurogenic inflammation
-sympathetic under activity and parasympathetic

116
Q

TX for cluster headaches

A

Oxygen inhalation, sumatriptan

117
Q

Age of onset for tension type headaches

A

10-20 yoa

118
Q

Cause of tension type headaches

A

Hypersensitivity of pain fibres from trigeminal nerve

119
Q

TX for tension type headaches

A

Mild TTH treated with ice, more severe with aspirin

120
Q

Meningitis vs encephalitis

A

M- infection of meninges and subarachnoid space

E- inflammation within brain

121
Q

Bacterial meningitis

A

-infants and children
-strep, s.pneumoniae, e.coli
Pathogens cross BBB into CSF then release toxins
-ICP occur due to black age of CSF

122
Q

Progressive symptoms of bacterial meningitis

A

Spinal rigidity, seizures, positive babinski reflex

123
Q

Viral meningitis

A

May be direct infection or secondary to disease such as measles, mumps, herpes

124
Q

Viral encephalitis

A

Virus can directly invade brain and cause inflammation, post infection may occur due to autoimmune response

125
Q

Multiple sclerosis

A

CNS demyelination, T and B cells cross BBB attack myelin, activation of micro Gaia

126
Q

Multiple sclerosis

A

CNS demyelination, T and B cells cross BBB attack myelin, activation of micro Gaia

127
Q

Guillain barr

A

PNS demyelination, secondary to other infections, recovery possible

128
Q

Demyelination disorders

A

Result of damage to myelin nerve sheath and affect on neural transmission

129
Q

Risk factors for multiple sclerosis

A

Epstein Barr virus, genetics

130
Q

Patho of MS

A

T and B cells cross BBB and attack myelin
-activation of microglia cells
Resulting in death of neurons, brain atrophy, primarily white tissue

131
Q

When does grey matter degeneration occur in MS

A

During later stages

132
Q

Initial symptoms of MS

A

-Paresthesia (burning or prickling sensations)

133
Q

diagnosis for MS

A

No single test to diagnose MS

134
Q

TX for MS

A

Corticosteroids, immunosuppressants, plasma exchange

135
Q

Patho for guilain barre syndrome

A

Demyelination of PN, secondary occurrence to respiratory or gastrointestinal infection

136
Q

Recovery for Giulian barre syndrome

A

Weeks to years, 30 percent have residualk weakness

137
Q

Symptoms of Giulian barre syndrome

A

Vary from tingling and weakness to leg paralysis and quadriplegia

138
Q

TX for Giulian barre syndrome

A

Intravenous immunoglobulin used during acute phase

139
Q

Most common NMJ disorder

A

Myasthenia Travis

140
Q

Myasthenia Travis

A

Chronic autoimmune disease
-antibodies against ACh receptors on postsynaptic membrane

141
Q

Thymoma

A

Tumour of thymus, associated with Myasthenia Travis

142
Q

Pathophysiology for Myasthenia Gravis

A

AChR are not recognized as self, thymoma forms a T cell dependant IgG autoantibodies which block binding site of AChR to acetylcholine
-destroy receptor site

143
Q

Manifestations of Myasthenia Gravis

A

Muscles of head area affected, dysphasia, diaphragm and chest wall muscles weaken

144
Q

Diagnosis of Myasthenia Gravis

A

Detection of anti-AChR antibodies

145
Q

TX for Myasthenia Gravis

A

Immunosuppressants, thymectomy for people with thymoma

146
Q

Primary tumours

A

Arise from brain substance
-do not metastasize readily bc there’s no lymph channels in brain substance

147
Q

Metastatic secondary tumours arise in

A

Organ systems outside brain and spread to brain

148
Q

Metastatic secondary tumours arise in

A

Organ systems outside brain and spread to brain

149
Q

Metastatic secondary tumours local effects:

A

compression causing decreased cerebral blood flow and inc ICP

150
Q

Symptoms of Metastatic secondary tumours

A

Seizures, visual disturbances

151
Q

What is more common primary or metastatic?

A

Metastatic tumours are 10 times more common Thant primary

152
Q

Primary Intracerebral tumours are called

A

Gliomas

153
Q

Risk factor for primary brain tumours

A

Ionizing radiation
-detaches electrons from other atoms as they pass thru matter

154
Q

How are primary brain tumours graded

A

From I to IV (IV being the most lethal)

155
Q

What is the most common glioma

A

Astrocytoma (75%)

156
Q

astrocytoma

A

Grade III and IV
-survival less than 5 years

157
Q

Oligodendroglioma

A

Slow growing, grade II
-primarily in white matter
-seizure is the first symptom

158
Q

Meningioma

A

Begins in dura mater, located on wings of sphenoid bone
-seizure is first symptom

159
Q

Ependymoma

A

More common in children, arise from ependymal cells with 70% change of tumours beginning in fourth ventricle

160
Q

Lower back pain affects the area between

A

Lower rib cage and gluteal muscles with pain often radiating into lower legs

161
Q

Acute LBP associated with

A

Muscle or ligament strain

162
Q

Chronic LBP

A

Includes degenerative disc disease, spondyloysis and spondylolisthesis

163
Q

Degenerative disc disease

A

Normal process of aging, genetic

164
Q

Spondylolysis

A

Occurs in the pars interarticularis of vertebral arch
-degeneration or fracture of PI

-wear on the cartilage/bones of the neck

165
Q

Spondylolisthesis

A

Froward slippage of a vertebra

166
Q

Spinal stenosis

A

Narrowing of spinal canal
-causing pressure on spinal nerves or cord

167
Q

Herniation of an intervertebral disk

A

Displacement of nucleus pulposus beyond intervertebral disc space

168
Q

Nucleus pulposus

A

Herniation = compresses spinal nerve = local/radiated pain

169
Q

Most affected discs

A

L4-L5, L5-S1

Pathophysiology (20 decks)

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