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patho > ch 16: disorders of CNS, PNS, and NMJ > Flashcards

ch 16: disorders of CNS, PNS, and 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 neural route, nerve plexus, nerves themselves, or neuromuscular junction

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3
Q

traumatic brain injury

A

TBI is primary cause of death and disability in individuals under age of 40
- 30% of all TBIs are kids, are usually from sports and rec activities

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4
Q

TBI (traumatic brain injury)

A

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

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5
Q

primary TBI

A
  • cause: indirect impact
  • injury can be focal (affecting one area; 2/3) or diffuse (more than 1 area; 1/3; diffuse axonal injury, DAI)
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6
Q

secondary TBI

A
  • cause: indirect result of primary injury
  • includes systemic responses and cascade of cellular and molecular cerebral events
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7
Q

TBI diagnosis

A

glasgow coma scale (GCS)

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8
Q

glasgow coma scale

A

3 categories:
1. eye (4)
2. verbal (5)
3. motor (6)

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9
Q

GCS 2 scores

A

eye: eye opening to pain
verbal: incomprehensible sounds
motor: extension to pain

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10
Q

GCS 3 scores

A

eye: eye opening to verbal command
verbal: inappropriate words
motor: flexion to pain

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11
Q

classification scores

A

severe head injury: score of 8 or less

moderate head injury: score of 9-12

mild head injury: score of 13-15

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12
Q

primary TBI

A

can be closed or open injury
- closed: more common, head sticking hard surface or moving object striking head, or blast waves, dura mater remains intact and brain tissue not exposed
- open: penetrating trauma or skull fracture, break in dura mater = brain tissue exposed

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13
Q

types of primary TBI

A
  1. primary focal closed
  2. primary focal open
  3. primary diffuse injury
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14
Q

types of primary focal closed TBIs

A
  1. coup/contrecoup
  2. contusion
  3. epidural (extradural) hematoma
  4. subdural hematoma
  5. intracerebral hematoma
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15
Q

primary focal closed brain injury

A

specific, observable brain injuries that occur in a precise location
- mild: 80% of cases
- severe: contusions, epidural, subdural, and hematomas

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16
Q

coup/contrecoup

A

coup = injury at site of impact
contrecoup = injury from brain bouncing back and hitting opposite side of skull

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17
Q

contusions (brain bruising)

A

compression of skull at point of impact produces blood leaking from injured vessel
- contusion as a result of blood leaking from injured vessel
- smaller contact area = more severe the injury
- edema forms, increased ICP = hemorrhages, edema, infarction, necrosis = tissue becomes “pulpy”
- frontal lobed most common injury site
- greatest injury effects: peak 18-36 hours after injury

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18
Q

contusions cont

A
  • diagnosis: glasgow coma scale, CT scan, MRI
  • TX: surgical removal of large contusions and areas of hemorrhage may be required
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19
Q

TBI primary focal hematomas

A
  1. epidural
  2. subdural (acute, chronic)
  3. intracerebral
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20
Q

epidural hematomas

A
  • skull fracture
  • hemiparesis
  • pupil dilation
  • loss of consciousness
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21
Q

subdural hemotomas

A

acute: fast/hemianopia
chronic: alcohol/craniotomy, membrane forms around hematoma

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22
Q

intracerebral hematomas

A
  • frontal temporal
  • penetrating sheering
  • pupil dilation
  • positive babinski
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23
Q

epidural hematomas

A

bleeding between dura mater and skull
- artery bleeding and hematoma
- temporal fossa most common site of EH

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24
Q

EH symptoms

A
  • generally lose consciousness
  • as hematoma grows = severe headache, confusion, seizure
  • hemiparesis (weakness or inability to move one side of body)
  • pupil dilation: injury prognosis good if treated before both pupils dilate

tx: medical emergency

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25
Q

dural

A

refers to dura mater

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26
Q

subdural hematomas

A

bleeding between dura mater and brain
- acute or chronic

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27
Q

acute SH

A

develop quickly, within hours
- hematomas grow, ICP rises, pressure is applied to bleeding veins (which assists in short term limitation)

symptoms: headache to confusion
- loss of consciousness, pupil dilation
- hemianopia = blindness over half of vision field
- anopia: aka blindness

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28
Q

chronic SH

A

develop over weeks to months
- common in alcohol abuse
- subdural mass bleeding = subdural space fills with blood
- vascular membrane forms around hematoma

symptoms:
- headaches and tenderness over hematomas
- worsening dementia, paratonia (rigidity)

TX: craniotomy to remove jelly-like blood

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29
Q

intracerebral hematomas

A

bleeding within the brain
- 2-3% of head injuries
- mainly in frontal and temporal lobes
- penetrating and shearing forces injure small blood vessels = growing mass/edema

symptoms:
- sudden rapid decrease in level of consciousness
- pupil dilation
- positive babinski reflex (big toe bends back and other toes fan out)

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30
Q

primary focal open TBI

A

compound skull fracture/missile injuries

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31
Q

compound skull fracture

A

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

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32
Q

causes of compound skull fractures

A
  1. crush: cutting or crushing whatever missile touches
  2. stretch: blood vessels and nerve damage without direct contact
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33
Q

compound skull fractures cont

A
  • symptoms: become unconscious

basilar skull fractures:
- usually caused by substantial blunt force trauma
- involves one of the bones that compose the base of the skull
- general spinal fluid leaking from ear or nose, blackened eyes

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34
Q

primary diffuse injury

A

diffuse brain injury is widespread in brain
- effects from high levels of acceleration and deceleration (whiplash) or rotational forces
- forces cause shearing of axonal fibers and white matter tracts
- the degree of shearing determines the cognitive consequences and extensive cognitive impairments

extensive cognitive impairments (survivors of vehicle accidents)

diagnosis: electron microscope to detect axonal damage

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35
Q

secondary brain injury

A

indirect result of primary brain injury: including trauma and stroke syndromes

both systemic and cerebral processes involved:
- systemic: hypotension, hypoxia, etc.
- cerebral: inflammation, edema, increase ICP

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36
Q

secondary brain injury cont

A

primary effects cause disruption to BBB = neuronal death

management:
- prevention of hypoxia, maintenance of perfusion pressure, and removal of hematomas

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37
Q

categories of traumatic brain injury

A
  1. mild
  2. moderate
  3. severe
38
Q

mild TBI (mild concussion)

A
  • characterized by immediate but transitory clinical manifestations
  • loss of consciousness less than 30 minutes
  • GCS (glasgow) score: 13-15
  • symptoms: headache, nausea, vomiting
  • diagnosis: blood test to determine need for CT scan
39
Q

moderate TBI (moderate concussion)

A
  • any loss of consciousness last more than 30 min up to 6 hrs
  • GCS score 9-12
  • permanent defects in arousal and attention
  • symptoms: confusion and amnesia lasting more than 24 hours, brain imaging is abnormal
40
Q

severe TBI (severe concussion)

A

characterized by loss of consciousness for more than 6 hours
- GCS score 3-8
- permanent damage to vegetative state to death
- signs: changes in pupillary reaction and cardiac and respiratory systems, decorticate or decerebrate posturing, brain imaging is abnormal, increased ICP occurs 4-6 days after injury
- symptoms: compromised coordinated movements, verbal and written communication
- goal of TX: maintain cerebral perfusion and promote neural protection

41
Q

complications of TBI

A

severity/brain location determines the probable locations

3 post-traumatic syndromes:
1. post-concussion syndrome
2. post-traumatic seizures
3. chronic traumatic encephalopathy (CTE)

42
Q

post-concussion syndrome

A
  • can last weeks to months after concussion
  • important to have first 24 hours of close observation
  • symptoms requiring further evaluation: drowsiness, confusion, vomiting, unequal pupils, CSF drainage from ears or nose, double vision
43
Q

post-traumatic seizures (epilepsy)

A
  • 10-20% of TBIs
  • highest risk with open brain injuries
  • molecular changes = sprouting of new hyperexcitable neural activity = increased seizures
44
Q

chronic traumatic encephalopathy (CTE)

A
  • progressive dementing disease that develops with repeated brain injury
  • associated with contact sports, and blast injuries with soldiers
  • tau neurofibrillary tangles occur in brain
  • consequences: violent behaviour, change in cognitive and motor function, depression, suicide
45
Q

decorticate posturing

A

flexing arms towards core and center of body

46
Q

decerebrate posturing

A

extension of arms

47
Q

spinal cord and vertebral injury

A

at risk: male gender (20-39) and older adults (79+ - because of falls)

can be primary or secondary injury

48
Q

primary spinal cord injury

A
  • initial mechanical trauma = immediate tissue damage
  • injury occurs if an injured spine does not receive adequate immobilization following trauma
  • injury to C1- 4 = life threatening due to loss of CV and respiratory function
49
Q

secondary spinal cord injury

A
  • disease causing process (vascular, cellular, biochemical) occurring within minutes and continues for weeks
  • hemorrhage appears in grey matter, result in death of entire grey matter at spinal level
  • edema - impaired circulation = ischemia
  • these symptoms occur at two cord segments above and below injury
  • cord swelling = increased dysfunction = difficult to distinguish permanent and temporary damage
  • death of oligodendrocytes = myelin degeneration
50
Q

vertebral injuries

A

vertebral fractures, dislocation, bone fragments = shearing and compression
- vertebral fracture easily due to torn supporting ligaments
- vertebrae misalignment and dislocation occurs
- vertebral injuries occur at most moveable portions of column

51
Q

hyperextension

A

disruption of intervertebral discs
- head moves up/back
- ligament compression and spinal cord compression

52
Q

flexion

A

vertebral wedge fracture
- head moves down
- stretched ligaments

53
Q

rotation

A

shearing force and rupture of ligament support

54
Q

manifestations of spinal cord/vertebral injury

A
  1. spinal shock
  2. neurogenic shock
55
Q

spinal shock

A

develops immediately after injury
- complete loss of function at or below level of injury
- hypothalamus cannot regulate body heat/person assumes temperature of aire (poikilothermic)
- generally lasts 7-20 days and returns with reflex emptying of bladder

56
Q

neurogenic shock

A

occurs with injury above T6
- unopposed parasympathetic activity (due to absence of sympathetic activity)
- result: vasodilation, hypotension

57
Q

primary headache syndrome

A

3 categories:
1. migraine
2. cluster
3. tension-type

58
Q

migraine

A
  • episodic, neurological headache lasting 4-72 hours
  • genetic and environmental components
  • classified as:
    1. with aura
    2. without aura
    3. chronic
  • occurrence in canada: 25% of women, 8% of men, 10% of children
59
Q

aura

A

begins as spreading neural hyperactivity in occipital brain region (visual processing regions)

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

60
Q

clinical phases of migraine

A
  1. premonitory phase: symptoms occur hours to days before onset of aura (tired, irritable)
  2. migraine aura
  3. headache phase: begins on one side of head - spread to entire head
  4. recovery phase: irritability, fatigue
61
Q

cluster headache

A

headache involving trigeminal nerve
- pain may alternate sides each episode
- severe throbbing
- up to 8 attacks a day
- cluster days followed by long periods of remission
- primarily in men age 20-50

pathophysiology:
- pain related to neurogenic inflammation
- sympathetic underactivity and parasympathetic activation

TX: oxygen inhalation, sumatriptan

62
Q

tension-type headaches

A

most common type of recurring headache
- age of onset: 10-20 years old
- gradual onset moves to sensation of tight band around head
- its is episodic over a period of days
- can develop into chronic if happening 15 days/month
- cause: hypersensitivity of pain fibers from trigeminal nerve
- TX: mild treated with ice, more severe treat with asprin

63
Q

meningitis

A

infection of meninges and subarachnoid space

64
Q

encephalitis

A

inflammation within brain

65
Q

inflammation introduction

A

pathogens infect CNS

mechanism:
- direct neural or glial infection
- inflammation = edema
- interruption of CSF pathways
- secretion of toxins

66
Q

bacterial meningitis

A

serious infections to which infants and children are susceptible
- streptococcus, s. pneumoniae and e coli are most common pathogens
- pathogens cross blood brain barrier, enter cerebrospinal fluid, multiply and release toxins
- ICP can occur due to blockage of CSF circulation
- progressive symptoms: spinal rigidity, seizures, positive babinski reflex

67
Q

viral meningitis

A

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

68
Q

viral encephalitis

A

virus can directly invade brain and cause inflammation
- post-infection encephalitis may occur due to an autoimmune response

69
Q

demyelinating disorders

A
  1. multiple sclerosis (MS)
    - CNS disorder
  2. Guillian-Barr
    - PNS disorder
70
Q

what are demyelinating disorders

A

result of damage to myelin sheath

71
Q

multiple sclerosis

A

chronic, immune-mediated inflammatory disease with CNS demyelination, scarring and loss of axons
- canada has one of the highest rates of MS
- onset: 20-40 yoa (more common in women)
- risk factors: epstein-barr virus (EBV), genetics

pathophysiology:
- diffuse progression in brain and spinal cord
- T and B cells cross BBB and attack myelin
- activation of microglia cells (CNS immune cells)
- result: death of neurons, brain atrophy with mainly white tissue atrophy
- gray matter degeneration occurs during later stages

manifestations:
- initial symptoms: paresthesia (burning or prickling sensations)
- exacerbation stages (relapses) followed by remission
- further exacerbations = progression of disease

TX:
- corticosteroids, immunosuppressants (both increased risk of infections)
- plasma exchange if patient doesn’t respond to steroids

72
Q

Guillain - Barre syndrome

A

pathophysiology:
- demyelination of peripheral nerves
- occurs secondary to respiratory or gastrointestinal infection
- recovery: weeks to years (30% have residual weakness)

symptoms:
- vary from tingling and weakness to leg paralysis, quadriplegia

73
Q

NMJ disoder

A

myasthenia gravis

74
Q

myasthenia gravis

A

most common NMJ disorder
- chronic autoimmune disease
- autoimmune: antibodies (IgG) against Ach receptors on postsynaptic membrane
- thymoma (tumour of thymus) associated with disorder

pathophysiology:
- AChR are not recognised as “self”
- result: Thymoma - formation of T-cell-dependant IgG autoantibodies which block binding site of AChR to ACh
- autoantibodies destroy receptor site

manifestation:
- muscles of head area earliest areas affected
- resulting dysphagia (difficulty swallowing) = risk of respiratory aspiration
- diaphragm and chest wall muscles weaken = impaired respiration

diagnosis:
- detection of anti-AChR antibodies

TX:
- immunosuppressants
- thymectomy for people with thymoma

75
Q

brain tumours

A

can be primary or metastatic

76
Q

oma

A

denotes tumor or cancer

77
Q

primary tumours

A

arise from brain substance
- do not metastasize readily because there is no lymph channels in brain substance
- AKA primary intracerebral tumours and gliomas
- 50-60% of adult brain tumours
- ionizing radiation only known risk factor (ionizing radiation detaches electrons from other atoms as they pass through matter)

78
Q

types of primary intracerebral tumours (gliomas)

A
  1. astrocytoma
  2. oligodendroglioma
  3. meningioma
  4. ependymoma
79
Q

astrocytoma

A

most common
- grade III and IV = survival less than 5 years

80
Q

oligodendroglioma

A
  • slow growing (grade II)
  • primarily in white matter
  • seizure first symptom
81
Q

meningioma

A
  • begins in dura mater
  • often located on wings of sphenoid bone
  • seizures first symptom
82
Q

ependymoma

A
  • more common in children
  • arise from ependymal cells with 70% of tumors begin in fourth ventricle
83
Q

metastatic (secondary) tumours

A

arise in organ systems outside brain and spread to the brain
- local effects of tumours are compression causing decreased cerebral blood flow and increased ICP
- symptoms: seizures, visual disturbances
- 10 times more common than primary
- 20-40% of people who have cancer metastasis to brain

84
Q

degenerative disorders of the spine

A
  1. lower pack pain
  2. degenerative disc disease (DDD)
  3. herniated intervertebral disc
85
Q

lower back pain

A
  • affects area between lower rib cage and gluteal muscles (muscles of buttck area) with pain often radiating into the lower legs
  • acute LBP associated with muscle or ligament strain
  • chronic LBP includes degenerative disc disease, spondylolysis and spondylolisthesis
86
Q

degenerative disc disease

A

process of normal aging, genetic
- spondylolysis
- spondylolisthesis
- spinal stenosis

87
Q

spondylolysis

A

occurs in the pars interarticularis (between the superior and inferior articular processes)
- degeneration or fracture of this joint

88
Q

spondylolisthesis

A

forward slippage of vertebrae

89
Q

spinal stenosis

A

narrowing of spinal canal
- pressure on spinal nerves or cord

90
Q
A

patho (4 decks)

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