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Y4R1 - Pediatrics I 👶 > L5: Acute Flaccid Paralysis > Flashcards

L5: Acute Flaccid Paralysis Flashcards

1
Q

Introduction to motor unit

A
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2
Q

Def of

  • Neuronopathy
  • Neuropathy
  • Myopathy
A
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3
Q

Def of Acute Flaccid Paralysis

A
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4
Q

Etiology of Acute Flaccid Paralysis

A
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5
Q

Etiology of Acute Flaccid Paralysis

  • Spinal Cord
A
  • Acute transverse myelitis
  • Trauma
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6
Q

Etiology of Acute Flaccid Paralysis

  • AHCs
A
  • Poliovirus & polio vaccination
  • Other neurotropic viruses e.g. CMV, EBV, HSV
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7
Q

Etiology of Acute Flaccid Paralysis

  • Peripheral Nerves
A
  • Guillain Barré syndrome
  • Critical illness neuropathy
  • Toxic neuropathy (arsenic, lead)
  • Diphtheritic neuropathy
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8
Q

Etiology of Acute Flaccid Paralysis

  • NMJ
A
  • Myasthenia gravis
  • Botulism
  • Organophosphate poisoning
  • Snakebite
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9
Q

Etiology of Acute Flaccid Paralysis

  • Muscles
A
  • Inflammatory myopathies
  • Critical illness myopathy
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10
Q

Etiology of Acute Flaccid Paralysis

  • Muscle Membrane
A
  • Familial periodic paralysis
  • 2ry hypokalemic paralysis
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11
Q

CP of Acute Flaccid Paralysis

A
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12
Q

CP of Acute Flaccid Paralysis

  • Weakness appears first in …..
A

Lower Limb

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13
Q

CP of Acute Flaccid Paralysis

  • Initial Complaint
A

Abnormal gait with proximal or distal leg weakness

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14
Q

CP of Acute Flaccid Paralysis

  • With Proximal Weakness
A
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15
Q

CP of Acute Flaccid Paralysis

  • With Distal Weakness
A
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16
Q

Physical Examination in Acute Flaccid Paralysis

A
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17
Q

Dx of Acute Flaccid Paralysis

A
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18
Q

INVx in Acute Flaccid Paralysis

A
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19
Q

INVx in Acute Flaccid Paralysis

  • Spinal Cord Lesions
A
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20
Q

INVx in Acute Flaccid Paralysis

  • Peripheral Nerve Lesions
A
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21
Q

INVx in Acute Flaccid Paralysis

  • NMJ Lesions
A

Repetitive nerve stimulation (RNS)

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22
Q

INVx in Acute Flaccid Paralysis

  • Muscle Lesions
A
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23
Q

Manamgment of Acute Flaccid Paralysis

A
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24
Q

Manamgment of Acute Flaccid Paralysis

  • ABC
A
  • Ensure airway protected and adequate ventilation
  • Check BP & HR
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25
Q

Manamgment of Acute Flaccid Paralysis

  • Specific TTT
A
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26
Q

Introduction to Guillian Barré Syndrome

A
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27
Q

Epidemeology of Guillian Barré Syndrome

A
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28
Q

Etiology of Guillian Barré Syndrome

A
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29
Q

Etiology of Guillian Barré Syndrome

  • Causative agents
A

It occurs 2 - 4 weeks after a benign febrile illness:

  • 2/3 of cases follow a respiratory or gastrointestinal infection
  • Campylobacter infection 20 - 30%
  • Others e.g. CMV, EBV, HSV

GBS has been reported to follow:

  • Vaccinations
  • Epidural anesthesia
  • Thrombolytic Agents
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30
Q

Pathogenesis of Guillian Barré Syndrome

A
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31
Q

Subtypes of Guillian Barré Syndrome

A
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32
Q

CP of Guillian Barré Syndrome

A
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33
Q

CP of Guillian Barré Syndrome

  • Motor
A
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34
Q

CP of Guillian Barré Syndrome

  • Sensory
A
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35
Q

CP of Guillian Barré Syndrome

  • Autonomic
A
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36
Q

CP of Guillian Barré Syndrome

  • CNs
A
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37
Q

INVx for Guillian Barré Syndrome

A
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38
Q

INVx for Guillian Barré Syndrome

  • CSF Analysis
A
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39
Q

INVx for Guillian Barré Syndrome

  • Electrophysiological Studies
A
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40
Q

Management of Guillian Barré Syndrome

A
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41
Q

Management of Guillian Barré Syndrome

  • Indication of PICU Admission
A
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42
Q

Management of Guillian Barré Syndrome

  • Specific TTT
A
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43
Q

Management of Guillian Barré Syndrome

  • IVIG
A
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44
Q

Management of Guillian Barré Syndrome

  • Advantages of IVIG
A

IVIG is the preferred immunomodulatory treatment as it is

  • easier to give
  • few side effects
  • the treatment can be implemented more quickly
  • good outcome as plasmapheresis
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45
Q

Management of Guillian Barré Syndrome

  • regimens of IVIG
A
46
Q

Management of Guillian Barré Syndrome

  • Plasmapheresis
A
47
Q

Prognosis of Guillian Barré Syndrome

A
48
Q

Incidence of Poliomyelitis

A
49
Q

Etiology of Poliomyelitis

A
50
Q

Type of Poliovirus

A

RNA Virus

51
Q

Serotypes of Poliovirus

A

There are 3 Serotypes of poliovirus (genus enterovirus)

  • Type 1 most frequently associated with epidemics and causes most paralytic manifestations
  • Types 2 & 3 usually associated with vaccine associated paralytic polio (VAPP)
52
Q

MOT of Poliovirus

A
  • Fecal-oral: absorption of poliovirus in the intestinal tract
  • Droplet (rare)
53
Q

Pathogenesis of Poliomyelitis

A
54
Q

Study CP, Dx & TTT of Polio

A
55
Q

Prevention of Poliomyelitis

A
56
Q

Prevention of Poliomyelitis

  • Advantages of OPV
A
  • Inexpensive
  • Easy to administer
  • Produces excellent immunity in the intestine (which helps prevent infection with wild virus in areas where it is endemic)
57
Q

Prevention of Poliomyelitis

  • IPV
A
  • Most industrialized countries have switched to IPV
  • which cannot revert
  • Either as the sole vaccine against poliomyelitis or in combination with OPV
58
Q

Risks of OPV

A

VAPP

59
Q

Def of VAPP

A
  • They are cases of AFP, which have residual weakness 60 days after onset of paralysis and vaccine related poliovirus is isolated from their stool
60
Q

Etiology of VAPP

A

In some recipient of OPV, there is genetic change (<1%) in the VP1 gene of vaccine virus

61
Q

CP of VAPP

A

It causes paralysis:

  • In recipient (recipient VAPP)
  • Among unimmunized close contacts (contact VAPP)
62
Q

Incidence of VAPP

A
  • 1 case of VAPP occurs after 2.3 million first doses, and after 12 million subsequent doses.
63
Q

Etiology of Traumatic Neuritis

A

Traumatic neuritis is caused by injection

64
Q

CP of Traumatic Neuritis

A
65
Q

Atrophy caused by a traumatic injection Never reaches the degree seen in polio

A

…

66
Q

Differences in calf circumference usually don’t exceed …….

A

0.5 - 1.5 cm.

67
Q

CP of Traumatic Neuritis

  • Site
A

may lead to AFP of the lower extremity.

68
Q

CP of Traumatic Neuritis

  • Associations
A
  • AFP is usually accompanied by pain in the gluteal region or along the affected leg.
  • Onset of AFP in the affected lower limb occurs from 1 hour - 5 days after injection in the gluteal region.
  • Fever is usually present before the onset of paralysis when injection is given for a pre-existing febrile illness.
69
Q

CP of Traumatic Neuritis

  • Atrophy
A

Atrophy may appear 40 - 60 days later

70
Q

Prognosis of Traumatic Neuritis

A

Gradual recovery with physiotherapy usually occurs within 3 - 9 months

71
Q

Compare between Poliomyelitis & Traumatic Neuritis in terms of:

  • Age
  • Reflexes
  • Ms Affected
  • Prognosis
A
72
Q

Def of Myasthenia Gravis

A

It’s an autoimmune disease of the neuro-muscular junction (NMJ) characterized by muscle weakness & fatigability that worsens with activity and improves with rest

73
Q

Etiology of Myasthenia Gravis

A
74
Q

Pathogenesis of Myasthenia Gravis

A
75
Q

CP of Myasthenia Gravis

A
76
Q

INVx for Myasthenia Gravis

A
77
Q

INVx for Myasthenia Gravis

  • Labs
A

Acetylcholine receptor antibody assays: +ve in 85 % of cases

  • the most helpful diagnostic investigation
78
Q

INVx for Myasthenia Gravis

  • Electrophysiological Studies
A
  • Repetitive nerve stimulation is abnormal with characteristic findings in 60%
79
Q

INVx for Myasthenia Gravis

  • Chest CT
A

Assessment of thymoma or thymic hyperplasia

80
Q

TTT for Myasthenia Gravis

A
81
Q

Def of Myasthenic Crisis

A

It is a serious life-threatening condition involving respiratory muscles

82
Q

TTT of Myasthenic Crisis

A
83
Q

Def of Transverse Myelitis

A

Acute demyelinating disorder of the spinal cord (other parts of CNS can affected)

84
Q

Incidence of Transverse Myelitis

A
  • Occurs in children aged ≥ 4 years
  • Most patients have only one episode of transverse myelitis
85
Q

Etiology of Transverse Myelitis

A

Commonly preceded by a viral infection or immunization

86
Q

Pathogenesis of Transverse Myelitis

A
87
Q

Pathogenesis of Transverse Myelitis

  • Most Commonly affected Site
A
  • Demyelination usually occurs at the thoracic leve causing problems with leg movement as well as bowel and bladder control
88
Q

DDx of Transverse Myelitis

A
89
Q

CP of Transverse Myelitis

A
90
Q

CP of Transverse Myelitis

  • Motor
A
91
Q

CP of Transverse Myelitis

  • Sensory
A
  • Back pain is common at the onset Els Neese
  • Sensory level of loss of sensation which is usually thoraci
92
Q

CP of Transverse Myelitis

  • Autonomic
A
  • Bladder and/or bowel incontinence
93
Q

TTT of Transverse Myelitis

A
94
Q

TTT of Transverse Myelitis

  • Acute Management
A
95
Q

Acute Management of Transverse Myelitis

  • 1st Line
A
96
Q

Acute Management of Transverse Myelitis
- 2nd Line

A
97
Q

Acute Management of Transverse Myelitis

  • Supportive Care
A

Management of bowl & bladder dysfunction

98
Q

Management of Transverse Myelitis

  • Long Term
A
  • Physical & occupational therapy to prevent contracture
  • Treatment of underlying cause
99
Q

Recovery of Transverse Myelitis

A
100
Q

Prognosis of Transverse Myelitis

A
101
Q

Pathogenesis of Botulism Toxicity

A
102
Q

Botulism Toxicity

  • Site
A

(in the colon/ in wounds / in food e.g, honey)

103
Q

CP of Botulism Toxicity

A
104
Q

CP of Botulism Toxicity

  • Non-Specific
A

Dry mouth

105
Q

CP of Botulism Toxicity

  • CN
A
106
Q

CP of Botulism Toxicity

  • Autonomic
A
  • Paralytic ileus advancing to severe constipation
  • Bladder distention advancing to urinary retention
  • Orthostatic hypotension
107
Q

CP of Botulism Toxicity

  • Additional Symptoms
A
  • Deep tendon reflexes are absent.
  • There is NO sensory loss.
  • There is NO fever
  • Consciousness is NOT impaired
108
Q

INVx for Botulism Toxicity

A
  • Toxin detection, serology
  • Electromyography (EMG), Nerve conduction study (NCS)
  • CSF examination is normal
109
Q

TTT of Botulism Toxicity

A
  • Antitoxin (Human botulism Ig)
  • Complete recovery takes weeks to months
110
Q

Diffrentiation between Different Types of AFP

A

Y4R1 - Pediatrics I 👶 (49 decks)

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