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2) Patho 2 > 13) GBS > Flashcards

13) GBS Flashcards

1
Q

GBS

A

Autoimmune disorder characterized by antibody-mediated demyelination

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2
Q

Why is the fact that schwann cells are spared w/GBS a good thing?

A

Allows for future recovery & re-myelinization

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3
Q

GBS is the most common cause of what?

A
  • Rapidly evolving motor paresis
  • Paralysis
  • Sensory deficits
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4
Q

What pop is GBS most common in?

A

Male young adults & people btwn ages 50-80

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5
Q

Sx’s of GBS

A
  • Flaccid paralysis
  • Areflexia
  • Respiratory compromise
  • Autonomic dysfxn
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6
Q

Explain the pathogensis of GBS

A
  • Schwann cells get attacked by the immune system
  • Inflammatory response is initiated–>Lymphocytes & macrophages
    • Macrophages strip myelin starting at the node of ranvier
  • Schwann cells divide & remyelinate nerves
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7
Q

W/flaccid paralysis, when does max weakness occur?

A

2-3wks after onset

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8
Q

What occurs in 50% of cases of fllaccid paralysis

A

Muscle weakness

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9
Q

What can pharyngeal & laryngeal weakness cause?

A

Dysphagia & subsequent aspiration

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10
Q

What occurs w/autonomic dysfxn?

A
  • BP & HR fluctuations
  • Excessive/No sweating
  • Flusing of face
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11
Q

Classic GBS (AIDP)

A

Acute Inflammatory Demyelinating Polyrediculoneuropathy

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12
Q

Describe the devo & progression of sx’s of AIDP

A

Fast from distal to proximal in a “stocking glove” manner

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13
Q

What other patho’s need to be r/o when dx’ing AIDP?

A
  • NMJ Pathos
    • Tick neuropathy
    • Toxic neuropathy
    • Myasthenia gravis
    • Neuromuscular blocking agents
  • CNS Pathos
    • Transverse myelitis
    • ASA syndrome
    • Polio
  • CVA
  • Metabolic disoders
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14
Q

NIH Criteria for Dx of GBS

A
  • Progressive, symmetric weakness in >1 limb
  • Loss of DTR
  • Sensory deficitd
  • Decr NCV
  • Tachycardia
  • Arrythmia
  • Labile BP
  • 1wk LP w/incr albumin & decr WBC
  • No fever
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15
Q

Is GBS a medical emergency?

A

Can be

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16
Q

Medical Management of GBS

A
  • Tx aimed at controlling the autoimmune response
  • Plasmapheresis to decr time on vent
  • IVIg
17
Q

Are corticosteroids effective for tx’ing GBS?

A

No

18
Q

When does recovery of GBS begin?

A

2-4wks after peak impairment

19
Q

What is the static phase?

A

Time between peak impairment & recovery

20
Q

How does GBS recovery occur?

A

From proximal to distal

21
Q

How long does GBS recovery take?

A

Wks to yrs

22
Q

Factors for a Good Prognosis

A
  • Younger age at onset
  • Shorter static phase
  • Inact axons
  • Less total impairment
  • No need for mechanical ventilation
23
Q

Factors for Poor Prognosis

A
  • Advanced age at onset
  • Longer static phase
  • Need for mechanical vent
  • Evidence of axonal degeneration
24
Q

AMAN

A

Acute Motor Axonal Neuropathy

25
Q

AMSAN

A

Acute Motor & Sensory Axonal Neuropathy

26
Q

Acute Autonomic Neuropathy

A

Postural hypotension, impaired sweating, & impaired B&B

27
Q

CIDP

A

Chronic Inflammatory Demyelinating Polyneuropathy

28
Q

Chronic Inflammatory Demyelinating Polyneuropathy

A

Chronic counterpart to GBS, but sx’s are more difuse, progression is slower, & can relapse-remit

29
Q

Who is CIDP more commonly dx’ed in?

A

Women & Young adults

30
Q

If GBS goes un-dx’ed, what can happen?

A

Severe permanent nerve damage

31
Q

Tx for GBS

A

Corticosteroids w/ or w/o immunosuppressants

32
Q

Long-term consequences of GBS tx

A
  • Mood swings
  • Fluid retention
  • Incr BP
  • Fx
  • OP
  • Bruising
  • Glaucoma
  • Weight gain
  • Incr infection risk
33
Q

Acute management of GBS

A
  • Skin care & positioning
  • ROM–>Splinting to prevent contractures
  • Respiratory management
  • Progress fxnl mobility
  • Pt & family ed
34
Q

What does rehab consist of?

A
  • Regain independence
  • Continue w/fxnl mobility
  • W/c mobility
  • Gait training w/BW support system or orthotics
  • Balance training
  • TherEx
  • Aquatic Therapy
35
Q

Is NMES effective & why?

A

No bc of demyelination

36
Q
A

2) Patho 2 (20 decks)

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