Exam 3 review updated
Spinal cord injury interventions on the field
Stabilize the spine, make sure airway is patent
Stay with the patient
Do not leave
Ask for help
Diagnostic tests for MG, GB, MS
Multiple sclerosis:
Mri (to identify Plaques or lesions in the brain and white (round areas, which is
inflammation). Lumbar puncture shows Oligoclonal bands present in the CSF fluid.
Medications: baclofen, cholinergics, atropine, alpha interferon, plasma pheresis, IG g,
Baclofen:
is a skeletal muscle relaxant used to decrease spasticity and improve bowel and
bladder function (In Multiple sclerosis and , ALS) , Reduces contractions.
Assess muscle spasticity before and periodically Observe for drowsiness, dizziness, or
ataxia
Instruct patient to change positions slowly to minimize orthostatic hypotension
Avoid alcohol or other CNS depressant or alcohol
AntiCholinesterance: meds that block the enzymes that causes ACH reuptake(i.e. MG)
Edrophonium, Neostigmine, and pyridostigmine
Take everyday at the same time. 30 min. before meals to increase muscle strength and to
prevent aspiration. Start in the AM.
Monitor for cholinergic crisis
Alpha interferon: such as Interferon beta-1a (Avenox)
prevents relapsing (Multiple sclerosis ) (numbing of the immune system)
It causes Flu-like symptoms and monitor for S&S on infection
,Plasmapheresis:
Re-transfusion of plasma. Removing the antibodies via centrifuge.
Watch out for S&S of hypovolemia
IVIGG: (Immunoglobulin G) Neutralizes antibodies. This is a transfusion. To not destroy the
myelin.
(MS, GB)
GUillian-Bare syndrome: prognosis, pathophysiology, treatments, s/s, nursing interventions
Prognosis: most people regain the strength, recovery may take up to 1-2 years.
( Depending of the regeneration of the Schwann cells)
Pathophysiology: Attack of the immune system to the myelin sheath after a viral
infection such as campylobacter jejuni, cytomegalovirus, Epstein-Barr virus,
Mycoplasma pneumoniae, Haemophilus influenzae, and HIV.
S/S:
Begins with muscle weakness and diminished reflexes of lower extremities
Weakness begins in the legs and may progress upwards
Cranial nerve demyelination can result in:
1. Optic nerve- blindness
2. Glossopharyngeal and vagus nerve clear secretions
3. Vagus nerve- cardiac instability- including tachycardia, bradycardia,
hypertension, orthostatic hypotension.
4. Miller- Fisher variant: includes paralysis of the ocular muscles, ataxia, areflexia
muscle
5. weakness, paresthesia, and ascending paralysis. Biggest issue is Respiratory.
Diagnosis:
Present with symmetrical weakness, diminishes reflexes and upward progression of
motor reflexes
History of a viral illness in the previous weeks 2-4 weeks prior
spinal tap show elevated protein levels in CSF without an increase in other cells
Evoked potential studies demonstrate a progressive loss of nerve velocity
Treatment
, TPE and IVIG – decrease circulating antibody levels and reduce the amount of time
the patient is immobilized and dependent on mechanical ventilation but we need to
monitor ECG
Alpha-adrenergic blocking agents to treat tachycardia and hypertension
IV fluid to manage hypotension
Nursing Interventions:
Two main reasons the pt may die:
1. Respiratory arrest
2. Immobility
Nursing Interventions: put patient on a cardiac monitor, assess gag reflex before
feeding, consult physical therapist, speech therapist , establish a method of
communication such as eye blink , referral to a support group, Turn the patient q2hr
to prevent pressure ulcers and skin breakdown to due immobility , increase fluid and
fiber for constipation, SCD , compression stocking, heparin to prevent DVT and PE,
move the pt slowly due to (orthostatic hypotension), prevent pneumonia (aspirate
secretions) by instruction patient to use Incentive spirometry, suction the patient to
remove secretion, intubation and mechanical ventilator to help with breathing.
Multiple Sclerosis : pathophysiology, s/s, risk factors, teaching to prevent relapse, nursing
interventions, teaching based on symptoms
Pathophysiology: autoimmune disease where sensitized T and B lymphocytes cross
the brain barrier and remain in the central nervous system and promote infiltration of
other agents that damage the immune system causing the immune system to attack
and causing inflammation that Destroy he myelin which insulates or protect the axon
and speed the conduction of implulses along the axon and also destroy the
oligodendroglial cells that produce myelin in the CNS. Destruction the myelin sheath
causes plaque or lesion formation in different part of the brain and decrease nerve
transmission speed.
Sign and symptoms:
Disease follow a benign course- symptoms are mild that the patient does not seek
treatment
Relapsing-remitting course- most common, with each relapse the patient recover but
the residual or remaining deficits can occur and accumulate over time and progress
to secondary remission.
Secondary progressive course- disease progression occur with or without relapses
Primary progressive course- Disabling symptoms steadily increases with rare plateau/
period of little change and temporary minor improvement. Disease showing
progression of disability right form the beginning without stopping and temporary
minor improvements
Spinal cord injury interventions on the field
Stabilize the spine, make sure airway is patent
Stay with the patient
Do not leave
Ask for help
Diagnostic tests for MG, GB, MS
Multiple sclerosis:
Mri (to identify Plaques or lesions in the brain and white (round areas, which is
inflammation). Lumbar puncture shows Oligoclonal bands present in the CSF fluid.
Medications: baclofen, cholinergics, atropine, alpha interferon, plasma pheresis, IG g,
Baclofen:
is a skeletal muscle relaxant used to decrease spasticity and improve bowel and
bladder function (In Multiple sclerosis and , ALS) , Reduces contractions.
Assess muscle spasticity before and periodically Observe for drowsiness, dizziness, or
ataxia
Instruct patient to change positions slowly to minimize orthostatic hypotension
Avoid alcohol or other CNS depressant or alcohol
AntiCholinesterance: meds that block the enzymes that causes ACH reuptake(i.e. MG)
Edrophonium, Neostigmine, and pyridostigmine
Take everyday at the same time. 30 min. before meals to increase muscle strength and to
prevent aspiration. Start in the AM.
Monitor for cholinergic crisis
Alpha interferon: such as Interferon beta-1a (Avenox)
prevents relapsing (Multiple sclerosis ) (numbing of the immune system)
It causes Flu-like symptoms and monitor for S&S on infection
,Plasmapheresis:
Re-transfusion of plasma. Removing the antibodies via centrifuge.
Watch out for S&S of hypovolemia
IVIGG: (Immunoglobulin G) Neutralizes antibodies. This is a transfusion. To not destroy the
myelin.
(MS, GB)
GUillian-Bare syndrome: prognosis, pathophysiology, treatments, s/s, nursing interventions
Prognosis: most people regain the strength, recovery may take up to 1-2 years.
( Depending of the regeneration of the Schwann cells)
Pathophysiology: Attack of the immune system to the myelin sheath after a viral
infection such as campylobacter jejuni, cytomegalovirus, Epstein-Barr virus,
Mycoplasma pneumoniae, Haemophilus influenzae, and HIV.
S/S:
Begins with muscle weakness and diminished reflexes of lower extremities
Weakness begins in the legs and may progress upwards
Cranial nerve demyelination can result in:
1. Optic nerve- blindness
2. Glossopharyngeal and vagus nerve clear secretions
3. Vagus nerve- cardiac instability- including tachycardia, bradycardia,
hypertension, orthostatic hypotension.
4. Miller- Fisher variant: includes paralysis of the ocular muscles, ataxia, areflexia
muscle
5. weakness, paresthesia, and ascending paralysis. Biggest issue is Respiratory.
Diagnosis:
Present with symmetrical weakness, diminishes reflexes and upward progression of
motor reflexes
History of a viral illness in the previous weeks 2-4 weeks prior
spinal tap show elevated protein levels in CSF without an increase in other cells
Evoked potential studies demonstrate a progressive loss of nerve velocity
Treatment
, TPE and IVIG – decrease circulating antibody levels and reduce the amount of time
the patient is immobilized and dependent on mechanical ventilation but we need to
monitor ECG
Alpha-adrenergic blocking agents to treat tachycardia and hypertension
IV fluid to manage hypotension
Nursing Interventions:
Two main reasons the pt may die:
1. Respiratory arrest
2. Immobility
Nursing Interventions: put patient on a cardiac monitor, assess gag reflex before
feeding, consult physical therapist, speech therapist , establish a method of
communication such as eye blink , referral to a support group, Turn the patient q2hr
to prevent pressure ulcers and skin breakdown to due immobility , increase fluid and
fiber for constipation, SCD , compression stocking, heparin to prevent DVT and PE,
move the pt slowly due to (orthostatic hypotension), prevent pneumonia (aspirate
secretions) by instruction patient to use Incentive spirometry, suction the patient to
remove secretion, intubation and mechanical ventilator to help with breathing.
Multiple Sclerosis : pathophysiology, s/s, risk factors, teaching to prevent relapse, nursing
interventions, teaching based on symptoms
Pathophysiology: autoimmune disease where sensitized T and B lymphocytes cross
the brain barrier and remain in the central nervous system and promote infiltration of
other agents that damage the immune system causing the immune system to attack
and causing inflammation that Destroy he myelin which insulates or protect the axon
and speed the conduction of implulses along the axon and also destroy the
oligodendroglial cells that produce myelin in the CNS. Destruction the myelin sheath
causes plaque or lesion formation in different part of the brain and decrease nerve
transmission speed.
Sign and symptoms:
Disease follow a benign course- symptoms are mild that the patient does not seek
treatment
Relapsing-remitting course- most common, with each relapse the patient recover but
the residual or remaining deficits can occur and accumulate over time and progress
to secondary remission.
Secondary progressive course- disease progression occur with or without relapses
Primary progressive course- Disabling symptoms steadily increases with rare plateau/
period of little change and temporary minor improvement. Disease showing
progression of disability right form the beginning without stopping and temporary
minor improvements
