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Clinical Med (Year 2) > Disorders of Peripheral Nervous System > Flashcards

Disorders of Peripheral Nervous System Flashcards

1
Q

What is the most common cause of acute evolving motor & sensory deficits?

A

Guillain-Barré syndrome (GBS)

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2
Q

What age groups are affected by GBS?

A
  • Young adults
  • 50-80 y/o
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3
Q

T/F: females are more likely to get GBS

A

False- slightly more males develop GBS

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4
Q

What is the etiology of GBS and what often precedes GBS?

A
  • Immune-mediated disorder
  • Acute infection often precedes
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5
Q

What are some common triggers for GBS?

A
  • Viral (Haemophilus influenza, Epstein-Barr, Cytomegalovirus)
  • Bacterial (Campylobacter jejuni)
  • Surgery
  • Vaccines
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6
Q

What is the pathogenesis of GBS in regards to demyelination of PNS?

A
  • Antibodies bind to myelin of Schwann cells
  • Macrophages respond to inflammatory signals & strip myelin from nerves
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7
Q

In regards to pathogenesis of GBS how does remyelination occur?

A

Schwann cells divide & remyelinate nerve axons

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8
Q

Why may there be axonal damage in an individual with GBS?

A

Inflammation

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9
Q

What axons are affected by GBS?

A
  • Motor
  • Motor and sensory
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10
Q

What is the clinical presentation of Acute Inflammatory demyelinating polyneuropathy (AIDP)?
A variant of GBS

A

progressive paralysis & areflexia due to demyelination

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11
Q

What is the clinical presentation of acute motor axonal neuropathy (AMAN)?
A variant of GBS

A

Axon involved, more severe, more respiratory involvement, more significant residual impairments

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12
Q

What is the clinical presentation of acute motor & sensory axonal neuropathy (AMSAN)?
A variant of GBS

A

Same as AMAN but with sensory involvement

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13
Q

What is the clinical presentation of Acute sensory ascending neuropathy (ASAN)?
A variant of GBS

A

Sensory > Motor

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14
Q

What is the clinical presentation of Miller Fisher syndrome?
A variant of GBS

A

Opthalmoplegia, ataxia, areflexia with sparing of strength

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15
Q

What is the clinical presentation of chronic inflammatory demyelinating polyneuropathy?
A variant of GBS

A

Slower onset, relapses & remissions or slow progression

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16
Q

What are the clinical manifestations of GBS?

A
  • Variation b/w subtypes
  • Ascending symmetrical weakness & distal sensory impairments
  • Flaccid paralysis
  • Absence of DTRs
  • Time from onset to peak impairment < 4 weeks
  • 30% require mechanical ventilation
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17
Q

What are the GBS stages and what occurs in each?

A
  • Progressive impairment (distal to proximal)
  • Static phase (2-4 wks)
  • Recovery (proximal to distal, may take months or years)
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18
Q

What symptoms are required for diagnosis of GBS?

A
  • Progressive weakness in > 1 extremity
  • Loss of DTRs
19
Q

What symptoms are supportive of a diagnosis of GBS?

A
  • Weakness developing rapidly ceasing to progress by week 4
  • Symmetric weakness
  • Mild sensory signs & symptoms
  • Facial weakness
  • Recovery starts 2-4 wks after progression ceases
  • Tachycardia, cardiac arrhythmias, & labile BP possbile
  • Absence of fever
20
Q

In order to diagnose GBS what features must the CSF have?

A
  • CSF protein levels increase after 1 week (continue to increase with serial exams)
  • CSF contains < 10 mononuclear leukocytes/mm3
21
Q

In order to diagnosis GBS what must the electrodiagnostic test show?

A

Nerve conduction velocity slowed

22
Q

What are some interventions for GBS?

A
  • Control of autoimmune responses
  • Mechanical ventilation
  • Prevention of effects of immobility
23
Q

What is the prognosis of GBS in regards to:
- Mortality rate?
- Recurrent form?
- 1 year?

A
  • Mortality rate: 5%
  • Recurrent form: 10%
  • 1 year: 67% complete recovery, 20% significant disability)
24
Q

What are the indications of a poor prognosis of GBS?

A
  • Older
  • Increase time before recovery begins
  • Need for artificial respiration
  • Reduced evoked potential (sign of axonal damage)
25
Q

What is polio?

A

Virus invades cell bodies of lower motor neurons in ventral horn of spinal cord resulting in asymmetric flaccid paresis or paralysis

26
Q

What is post- polio syndrome?

A

New neuromuscular symptoms occurring decades (average 25 years) after recovery from the acute paralytic episode

27
Q

How many survivors are there of acute poliomyelitis in US? And how many will develop post-polio?

A
  • 1.63 million survivors
  • 1/4 to 1/2 will develop post-polio
28
Q

What is the etiology of post-polio syndrome?

A
  • Denervated muscles were reinnervated by collateral sprouting from surviving nerves
  • Axons innervating more muscle fibers than originally intended
  • Nervous system can no longer support giant motor units
  • Prune back axonal sprouts
29
Q

What are the clinical manifestations of post-polio syndrome?

A
  • Declining muscle strength in previously affected & unaffected muscles
  • Myalgia
  • Joint pain
  • Muscle atrophy
  • excessive fatigue
30
Q

How is post-polio diagnosed?

A
  • Clinical
  • EMG
  • Muscle biopsy
31
Q

What are the intervention strategies for post-polio syndrome?

A
  • Treat symptoms
  • Modify lifestyle
  • Surgery (for deformities)
  • Avoid working to fatigue
32
Q

What is the prognosis of post-polio syndrome?

A
  • Slowly progressive
  • Stable period (3-10 years)
  • Decreased function & quality of life
33
Q

What is Myasthenia Gravis?

A
  • Motor end plate disorder
  • Most common neuromuscular transmission disorder
34
Q

What is Myasthenia Gravis characterized by?

A

Fluctuating weakness & fatiguability of skeletal muscles

35
Q

What is the age of onset of Myasthenia Gravis?

A
  • Males: 50 to 60 years
  • Females: 20 to 30 years
36
Q

Is Myasthenia Gravis more common in females or males?

A

Females > males (3:2)

37
Q

What is the etiology of Myasthenia Gravis?

A

Autoimmune disorder affecting neuromuscular junction & motor end plate

38
Q

What is the pathogenesis of Myasthenia Gravis?

A
  • Anti-Ach receptor antibodies (block receptor site & cause endocytosis of receptor)
  • Acetylcholine receptors decreased & flattened which decreases efficiency of neuromuscular transmission
  • so failure of nerve impulses to cross neuromuscular junction to stimulate muscle contraction
  • Thymus may trigger the autoimmune response
39
Q

What are the clinical manifestations of Myasthenia Gravis?

A
  • Skeletal muscle fatigue & weakness (Activity causes fatigue & rest restores activity)
  • Weak neck & facial muscles
40
Q

Patients with Myasthenia Gravis have weak neck & fascial muscles. How does this manifest?

A
  • Diplopia
  • Ptosis
  • Weak neck muscles
  • Nasal speech
  • Dysphagia
  • Nasal regurgitation
  • Aspiration of food
41
Q

What are the three diagnostic methods of Myasthenia Gravis?

A
  1. Immunologic - Detect anti-Ach receptor antibodies
  2. Pharmacologic - acetylcholinesterase inhibitor (blocks Ach reuptake) Improves strength & endurance
  3. Electrophysiological - repeated stimulation shows a rapid decrease in motor action potential amplitude
42
Q

What are some interventions for Myasthenia Gravis?

A
  • AChE inhibitor meds
  • Surgery (removal of thymus)
  • Corticosteroids
  • Plasmapheresis
43
Q

What is the prognosis of Myasthenia Gravis?

A
  • Slowly progressive disorder (periods of exacerbation & remission)
  • Myasthenia crisis
44
Q

What is Myasthenia crisis?

A
  • medial emergency
  • Respiratory muscle weakness

Clinical Med (Year 2) (17 decks)

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