L5: Acute Flaccid Paralysis Flashcards
(110 cards)
1
Q
Introduction to motor unit
A
2
Q
Def of
- Neuronopathy
- Neuropathy
- Myopathy
A
3
Q
Def of Acute Flaccid Paralysis
A
4
Q
Etiology of Acute Flaccid Paralysis
A
5
Q
Etiology of Acute Flaccid Paralysis
- Spinal Cord
A
- Acute transverse myelitis
- Trauma
6
Q
Etiology of Acute Flaccid Paralysis
- AHCs
A
- Poliovirus & polio vaccination
- Other neurotropic viruses e.g. CMV, EBV, HSV
7
Q
Etiology of Acute Flaccid Paralysis
- Peripheral Nerves
A
- Guillain Barré syndrome
- Critical illness neuropathy
- Toxic neuropathy (arsenic, lead)
- Diphtheritic neuropathy
8
Q
Etiology of Acute Flaccid Paralysis
- NMJ
A
- Myasthenia gravis
- Botulism
- Organophosphate poisoning
- Snakebite
9
Q
Etiology of Acute Flaccid Paralysis
- Muscles
A
- Inflammatory myopathies
- Critical illness myopathy
10
Q
Etiology of Acute Flaccid Paralysis
- Muscle Membrane
A
- Familial periodic paralysis
- 2ry hypokalemic paralysis
11
Q
CP of Acute Flaccid Paralysis
A
12
Q
CP of Acute Flaccid Paralysis
- Weakness appears first in …..
A
Lower Limb
13
Q
CP of Acute Flaccid Paralysis
- Initial Complaint
A
Abnormal gait with proximal or distal leg weakness
14
Q
CP of Acute Flaccid Paralysis
- With Proximal Weakness
A
15
Q
CP of Acute Flaccid Paralysis
- With Distal Weakness
A
16
Q
Physical Examination in Acute Flaccid Paralysis
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17
Q
Dx of Acute Flaccid Paralysis
A
18
Q
INVx in Acute Flaccid Paralysis
A
19
Q
INVx in Acute Flaccid Paralysis
- Spinal Cord Lesions
A
20
Q
INVx in Acute Flaccid Paralysis
- Peripheral Nerve Lesions
A
21
Q
INVx in Acute Flaccid Paralysis
- NMJ Lesions
A
Repetitive nerve stimulation (RNS)
22
Q
INVx in Acute Flaccid Paralysis
- Muscle Lesions
A
23
Q
Manamgment of Acute Flaccid Paralysis
A
24
Q
Manamgment of Acute Flaccid Paralysis
- ABC
A
- Ensure airway protected and adequate ventilation
- Check BP & HR
25
Manamgment of **Acute Flaccid Paralysis**
- Specific TTT
26
Introduction to **Guillian Barré Syndrome**
27
Epidemeology of **Guillian Barré Syndrome**
28
Etiology of **Guillian Barré Syndrome**
29
Etiology of **Guillian Barré Syndrome**
- Causative agents
**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
30
Pathogenesis of **Guillian Barré Syndrome**
31
Subtypes of **Guillian Barré Syndrome**
32
CP of **Guillian Barré Syndrome**
33
CP of **Guillian Barré Syndrome**
- Motor
34
CP of **Guillian Barré Syndrome**
- Sensory
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CP of **Guillian Barré Syndrome**
- Autonomic
36
CP of **Guillian Barré Syndrome**
- CNs
37
INVx for **Guillian Barré Syndrome**
38
INVx for **Guillian Barré Syndrome**
- CSF Analysis
39
INVx for **Guillian Barré Syndrome**
- Electrophysiological Studies
40
Management of **Guillian Barré Syndrome**
41
Management of **Guillian Barré Syndrome**
- Indication of PICU Admission
42
Management of **Guillian Barré Syndrome**
- Specific TTT
43
Management of **Guillian Barré Syndrome**
- IVIG
44
Management of **Guillian Barré Syndrome**
- Advantages of IVIG
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
45
Management of **Guillian Barré Syndrome**
- regimens of IVIG
46
Management of **Guillian Barré Syndrome**
- Plasmapheresis
47
Prognosis of **Guillian Barré Syndrome**
48
Incidence of **Poliomyelitis**
49
Etiology of **Poliomyelitis**
50
Type of Poliovirus
RNA Virus
51
Serotypes of Poliovirus
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
MOT of Poliovirus
* Fecal-oral: absorption of poliovirus in the intestinal tract
* Droplet (rare)
53
Pathogenesis of **Poliomyelitis**
54
Study CP, Dx & TTT of Polio
55
Prevention of **Poliomyelitis**
56
Prevention of **Poliomyelitis**
- Advantages of OPV
- Inexpensive
- Easy to administer
- Produces excellent immunity in the intestine (which helps prevent infection with wild virus in areas where it is endemic)
57
Prevention of **Poliomyelitis**
- IPV
- Most industrialized countries have switched to IPV
- which cannot revert
- Either as the sole vaccine against poliomyelitis or in combination with OPV
58
Risks of **OPV**
VAPP
59
Def of **VAPP**
- 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
Etiology of **VAPP**
In some recipient of OPV, there is genetic change (<1%) in the VP1 gene of vaccine virus
61
CP of **VAPP**
It causes paralysis:
- In recipient (recipient VAPP)
- Among unimmunized close contacts (contact VAPP)
62
Incidence of **VAPP**
- 1 case of VAPP occurs after 2.3 million first doses, and after 12 million subsequent doses.
63
Etiology of **Traumatic Neuritis**
Traumatic neuritis is caused by injection
64
CP of **Traumatic Neuritis**
65
Atrophy caused by a traumatic injection Never reaches the degree seen in polio
...
66
Differences in calf circumference usually don't exceed .......
0.5 - 1.5 cm.
67
CP of **Traumatic Neuritis**
- Site
may lead to AFP of the lower extremity.
68
CP of **Traumatic Neuritis**
- Associations
- 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
CP of **Traumatic Neuritis**
- Atrophy
Atrophy may appear 40 - 60 days later
70
Prognosis of **Traumatic Neuritis**
Gradual recovery with physiotherapy usually occurs within 3 - 9 months
71
Compare between **Poliomyelitis** & **Traumatic Neuritis** in terms of:
- Age
- Reflexes
- Ms Affected
- Prognosis
72
Def of **Myasthenia Gravis**
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
Etiology of **Myasthenia Gravis**
74
Pathogenesis of **Myasthenia Gravis**
75
CP of **Myasthenia Gravis**
76
INVx for **Myasthenia Gravis**
77
INVx for **Myasthenia Gravis**
- Labs
Acetylcholine receptor antibody assays: +ve in 85 % of cases
- the most helpful diagnostic investigation
78
INVx for **Myasthenia Gravis**
- Electrophysiological Studies
- Repetitive nerve stimulation is abnormal with characteristic findings in 60%
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INVx for **Myasthenia Gravis**
- Chest CT
Assessment of thymoma or thymic hyperplasia
80
TTT for **Myasthenia Gravis**
81
Def of **Myasthenic Crisis**
It is a serious life-threatening condition involving respiratory muscles
82
TTT of **Myasthenic Crisis**
83
Def of **Transverse Myelitis**
Acute demyelinating disorder of the spinal cord (other parts of CNS can affected)
84
Incidence of **Transverse Myelitis**
- Occurs in children aged ≥ 4 years
- Most patients have only one episode of transverse myelitis
85
Etiology of **Transverse Myelitis**
Commonly preceded by a viral infection or immunization
86
Pathogenesis of **Transverse Myelitis**
87
Pathogenesis of **Transverse Myelitis**
- Most Commonly affected Site
- Demyelination usually occurs at the thoracic leve causing problems with leg movement as well as bowel and bladder control
88
DDx of **Transverse Myelitis**
89
CP of **Transverse Myelitis**
90
CP of **Transverse Myelitis**
- Motor
91
CP of **Transverse Myelitis**
- Sensory
- Back pain is common at the onset Els Neese
- Sensory level of loss of sensation which is usually thoraci
92
CP of **Transverse Myelitis**
- Autonomic
- Bladder and/or bowel incontinence
93
TTT of **Transverse Myelitis**
94
TTT of **Transverse Myelitis**
- Acute Management
95
Acute Management of **Transverse Myelitis**
- 1st Line
96
Acute Management of **Transverse Myelitis**
- 2nd Line
97
Acute Management of **Transverse Myelitis**
- Supportive Care
Management of bowl & bladder dysfunction
98
Management of **Transverse Myelitis**
- Long Term
* Physical & occupational therapy to prevent contracture
* Treatment of underlying cause
99
Recovery of **Transverse Myelitis**
100
Prognosis of **Transverse Myelitis**
101
Pathogenesis of **Botulism Toxicity**
102
**Botulism Toxicity**
- Site
(in the colon/ in wounds / in food e.g, honey)
103
CP of **Botulism Toxicity**
104
CP of **Botulism Toxicity**
- Non-Specific
Dry mouth
105
CP of **Botulism Toxicity**
- CN
106
CP of **Botulism Toxicity**
- Autonomic
* Paralytic ileus advancing to severe constipation
* Bladder distention advancing to urinary retention
* Orthostatic hypotension
107
CP of **Botulism Toxicity**
- Additional Symptoms
* Deep tendon reflexes are absent.
* There is NO sensory loss.
* There is NO fever
* Consciousness is NOT impaired
108
INVx for **Botulism Toxicity**
* Toxin detection, serology
* Electromyography (EMG), Nerve conduction study (NCS)
* CSF examination is normal
109
TTT of **Botulism Toxicity**
* Antitoxin (Human botulism Ig)
* Complete recovery takes weeks to months
110
Diffrentiation between Different Types of **AFP**
