Chap 29, 30, 42, 43 Flashcards
Guillian-Bare Syndrom (GBS)
AUTOIMMUNE DISEASE
- Causes an acute peripheral nervous system disorder results in a flaccid paralysis of the skeletal muscle and loss of muscle reflexes
- Paralysis of the diaphragm and ventricular failure can develop= needing to be on mechanical vent.
- “weak legs”
Polyneuropathy
Flaccid paralysis of the skeletal muscle and loss of muscle reflexes
Major Pathologic or structural changes of the lungs with GBS
- Mucous accumulation
- Airway obstruction
- Alveolar Consolidation
- Atelectasis
Development of GBS is unknown, but they do know that it is from an
immune response of foreign antigens that attack nerve tissue and lymphocytes
-Macrophages attack and strip off the myelin sheath of the peripheral nerves and leave swelling and frags of neural axons
Onset of GBS
1-4 weeks after a febrile episode caused by a mild resp. or gastrointestinal viral or bacterial infection
Clinical History of GBS
- Symmetric muscle weakness in distal extremities or dysesthesias (unpleasant, abnormal sense of touch), accompanied by paresthesia (tingling, burning, shockline sensation)
- Pain (especially lower back, butt, legs)
- Numbness
Dysesthesias
unpleasant, abnormal sense of touch
Paresthesia
tingling, burning, shockline sensation
Muscle paralysis in GBS
spreads upwards starting at the (g)round to (b)rain
-Ascending paralysis
GBS paralysis spreads in what time period
In single day or several days
- peaks about 2 weeks
- 90% full recovery, as long as 3 years
Diagnosis of GBS
Pts clinical hx
cerebrospinal fluid findings
EMG
Nerve conduction studies (NCS)= increase and protein
EMG and Nerve Conduction Studies (NCS) show what with GBS
Acute polyneuropathy with demyelinating antibodies- associated with axonal subtypes of GBS
Treat GBS with what
Corticosteroid
GBS common in
Higher chance in whites 50 years old and older
-Similar male and female
Acute Vent. Failure averages
Vital Capacity < 20ml/kg
NIF < -25cmH2O
pH < 7.32 or
PaCo2 > 45 mmHg
We measure vital capacity with
NIF
GBS potential medical emergency
30% -> acute vent. failure and require mechanical vent..
-Stabalize vitals and supportive care, frequent measurements FVC and MIP
GBS primary treatment
- Plasma pheresis
2. Intravenous immune globulin
Plasma pheresis
Removes antibodies from plasma that contributes to the immune system attack on peripheral nerves
Intravenous immune globulin
Blood product that contains IgG from donors
-Lasts 2weeks - 3 months
Added risk of thromboembolism increase=
patient receives anticoagulants , elastic stockings, and passive range of motion exercises (ev. 3-4 hours) turn patient frequently
Myasthenia Gravis
Most common chronic disorder of the neuromascular junction, only affects myoneural (motor) junction, sensory function not lost.
-Interferes with acetylcholine (AcH) between the axon terminal and receptor sites of voluntary muscles
Hallmark clinical features of Myasthenia Gravis
Fluctuating Skeletal muscle weakness usually improves following rest
-Fatigue and weakness usually improves as well with rest
2 clinical types of Myasthenia Gravis
- Ocular
2. Generalized