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Summary Nur 265 Exam 3 Study Guide

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October 17, 2024
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ADVANCED MED SURG STUDY GUIDE EXAM 3

Unit 7: Complex Mobility, Sensation, and Cognition




Guillain- Barre Syndrome GBS

Pathophysiology A rare acute inflammatory (autoimmune) disorder that affects the
axons and or myelin of the PNS resulting in ascending muscle
weakness or paralysis from the feet up.

Clinical CM: Progressive/ rapid symmetrical ascending muscle weakness,
Manifestations/ lower extremity weakness, pain.
Complications
Complications: Respiratory failure, cardiac dysrhythmias, DVT,
respiratory acidosis, autonomic dysreflexia.

Autonomic dysreflexia: CM: severe hypertension, bradycardia,
profuse sweating, flushing, blurred vision, spots in pt. visual field,
nasal congestion, severe throbbing HA, and apprehension.

Etiology/ Risk The immune system overreacts to an infection and destroys the myelin
factors sheath. Involves cranial and peripheral nerves.

RF: Hx of respiratory or GI infection in the past 1-4 weeks,
vaccination, surgery.
Tests/ Electromyography (EMG)- measures nerve activity in muscles
Diagnostics Electroencephalogram (EEG)- measures electrical activity of the brain
Spinal tap- CSF reveals elevated protein level
Therapeutic Plasmapheresis- plasma exchange to remove antibodies.
Management IVIG- delivers donor plasma with health antibodies.

,Nursing/ Assessment PRIORITY: Airway, cardiac status! Intubation tray should be at
bedside- if resp. status worsens prepare for ventilator. Place on
tele!

Assess and monitor resp. and cardiac status closely. Potential for
sensation changes, monitor for dysphasia. If BP high, sit pt. up and
assess for urine retention, need for cath, fecal impaction, bowel
needs, etc.

Provide pt. and family with support. Needs interdisciplinary team.




Myasthenia Gravis

Pathophysiology A neuromuscular disease characterized by considerable weakness
and abnormal fatigue of the voluntary muscles. A defect occurs in
the transmission of nerve impulses at the myoneural junction. This
results in descending muscle weakness or paralysis from the head
down.
Clinical CM: Muscle weakness and fatigue, difficulty chewing and swallowing,
Manifestations/ dysphagia, ptosis, diplopia, weak hoarse voice, difficulty breathing,
Complications diminished breath sounds.

Complications: Respiratory paralysis and failure.
Etiology/ Risk Caused by insufficient secretion of acetylcholine, unresponsiveness of
factors the muscle fibers to acetylcholine, and excessive secretion of
cholinesterase.
Tests/ Anticholinesterase testing with edrophonium to diagnosis myasthenia
Diagnostics gravis or to distinguish cholinergic crisis from myasthenic crisis.

Edrophonium testing parameters: An edrophonium injection
temporarily improves the condition when pt. is in myasthenic
crisis; temporarily worsens the condition when pt. is in cholinergic
crisis.

Considerations: Edrophonium can cause bronchospasms,
laryngospasm, hypotension, bradycardia, and cardiac arrest. Have the
antidote, atropine, available.

ANA test
Therapeutic Anticholinesterase medications to relieve muscle weakness:
Management Neostigmine bromide and pyridostigmine

, Nursing/ Assessment PRIORITY: Airway! Monitor for resp. failure! Have Ambu bag,
intubation tray, and suction at bedside!

Monitor for myasthenic and cholinergic crisis and speech and
swallowing abilities! At risk for aspiration during meals. Teach pts to
avoid stress and ETOH and space out activities to conserve energy and
restore muscle strength. Wear medical alert bracelet.

Myasthenia crisis- Affect SNS.
CM: Increase HR, RR, BP, bowel/ bladder incontinence, dyspnea,
severe generalized muscle weakness; absent cough and swallow reflex.
Usually caused by undermedication, stress/ overexertion, or occurs
after resp. infection. Treat with edrophonium (cholinergic drug/
anticholinesterase drug).

Cholinergic crisis- Affects PNS.
CM: Abdominal cramps, n/v, diarrhea, hypotension, increased
bronchial secretions and perspiration, bronchospasm, wheezing, and
bradycardia. Medication induced (OD on meds). Treat with IV atropine
(anticholinergic drug).




Meningitis

Pathophysiology Infection of the meninges of the brain and spinal cord, specifically the
pia mater and arachnoid. The infectious organism enters the CNS
directly or via the bloodstream. Can spread to cranial and spinal nerves
causing irreversible damage.
Clinical CM: Decreased LOC, disoriented, photophobia, nystagmus,
Manifestations/ hemiparesis, hemiplegia, decreased muscle tone, cranial nerve
Complications dysfunction, memory changes, severe HA, myalgia, n/v, fever, chills,
tachycardia

Indications of meningeal irritation:
Kernig sign- loss of the ability of a supine client to straighten the leg
completely when it is fully flexed at the knee and hip.

Brudzinski sign- Involuntary flexion of the hip and knee when the neck
is passively flexed.

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