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NUR 333 Final Exam Spring 2017
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NUR 333 Final Exam-Spring 2017Chronic Neuromuscular Disorders
Guillain-Barre Syndrome
Etiology and Pathophysiology
ASCENDING PARALYSIS
Autoimmune disorder preceded by infection, trauma or surgery
Acute, rapidly progressing, and potentially fatal form of polyneuritis
Clinical Manifestations
Symptoms appear SYMMETRICAL and develop in days to weeks
Paresthesia (numbness and tingling) in the extremities
Hypotonia (reduced muscle tone) and areflexia (lack of reflexes – in arms and legs)
Orthostatic hypotension, hypertension, and vagal responses (bradycardia, heart block, asystole)
Bowel and bladder dysfunction, diaphoresis, facial flushing
Pain –paresthesias, muscular aches and cramps, and hyperesthesia (increased sensitivity)
Respiratory failure as paralysis progresses upwards
Disease does not affect level of consciousness, cognition or pupillary constriction/dilation – mind is intact
Collaborative Care
During acute phase:
– Monitor the ascending paralysis; assess respiratory function; monitor arterial blood gases (ABGs); and assess
the gag, corneal, and swallowing reflexes. Reflexes are usually decreased or absent.
Carefully assess swallowing and gag reflex and take measures to prevent aspiration – HOB elevated
Plasma exchange (plasmapheresis): removes circulating antibodies thought to be responsible for the disease –
monitor for hypovolemia, hypokalemia – is only useful during first 2 weeks
– Plasma is separated from the whole blood and blood cells are returned to the patient without the plasma
– Interventions: weighing the patient before and after procedure, caring for the shunt or venous access site and
preventing complications, provide information and reassurance
– Cannot go back to corticosteroids after plasmapheresis
High dose immunoglobin therapy (Sandoglobulin)
– ADE: chills, mild fever, myalgia, headache, anaphylaxis, aseptic meningitis, retinal necrosis
Myasthenia Gravis
Etiology and Pathophysiology
FACIAL/MUSCLE WEAKNESS – eyes, eyelids, swallowing, speaking, breathing
Alterations/blockage of acetylcholine at neuromuscular junction prevents muscle contraction
Autoimmune disease with fluctuating weakness of certain skeletal muscle groups
Clinical Manifestations
Muscles are generally the strongest in the morning and become exhausted with continued activity – periods of rest
are necessary
Difficulty breathing (weakness to chest wall muscles), impaired speech and swallow, eyelid drooping (ptosis), double
vision, fatigue, weakness
Exacerbations can be caused by emotional stress, trauma, temperature extremes, hypokalemia
Prognosis: some patients have short-term remissions, others stabilize, others may have severe
Myasthenic Crisis
Acute exacerbation of muscle weakness, triggered by infection, surgery, emotional distress, drug overdose or
inadequate drugs. The major complications of MG result form muscle weakness in areas that affect breathing and
swallowing = intubation and ventilator!! Emergency!!
– Can results in aspiration, respiratory insufficiency and respiratory infection
– Keep bag-valve-mask equipment for oxygen administration, and suction equipment at bedside
– Symptoms improve with Tensilon Test (ACh is injected and breathing improves)
Cholinergic Crisis
Symptoms worsen with Tensilon Test – INCREASES WEAKNESS and does not improve muscle tone
Too much cholinesterase inhibitor drugs
,Diagnosis
Blood test to detect the presence of immune molecules or acetylcholine receptor antibodies
Tensilon test: reveals improved muscle contraction after IV injection of Edrophonium chloride (Tensilon)
– In case of adverse effects of Tensilon, Atropine should be administered
Collaborative Care
Drug Therapy:
– Anticholinesterase agents (neostigmine, pyridostigmine) – help improve neuromuscular transmission and
increase muscle strength - report nausea to HCP
– Corticosteroids (Prednisone): is used to suppress the immune response
Plasmapheresis: short term improvement indicated for patients in crisis or in preparation for surgery when
corticosteroids must be avoided – cannot go back to corticosteroids after doing plasmapheresis – last resort
Surgery: thymus gland removal may cure individuals
Multiple Sclerosis
Chronic progressive, degenerative disorder of the CNS – onset between 20 – 50 years old
Related to infectious (viral), immunologic, and genetic factors
Clinical Manifestations
Numbness, weakness, tingling feeling in arms and legs
Weakness or paralysis of the limbs, the trunk, or the head; diplopia (double vision); scanning speech; and spasticity
of the muscles that are chronically affected, gait and balance problems
Numbness and tingling, patchy blindness (scotomas), blurred vision, vertigo, tinnitus, decreased hearing
Lhermitte’s sign: electric shock radiating down the spine or into the limbs with flexion of the neck.
Fatigue that is aggravated by heat, humidity, deconditioning, and medication side effects
Constipation, spastic bladder incontinence and dribbling, flaccid bladder resulting in urinary retention
Short attention span, poor judgement and memory difficulty – patient remains intellectually intact
Speech and swallowing symptoms: slurred or difficult-to-understand speech, trouble chewing and swallowing,
fatigue is a common and bothersome symptom of MS progresses. It is often worse in the late afternoon
Diagnostic Studies
MRI of the brain and spinal cord may show plaques, inflammation, atrophy, and tissue breakdown/destruction
CSF analysis (lumbar puncture/spinal tap) may show an immunoglobulin G
To be diagnosed with MS patient must have:
– Evidence of at least two inflammatory demyelinating lesions in at least two different locations in CNS
– Damage or an attack occurring at different times (usually 1 month or more apart)
– All other possible diagnoses ruled out
Collaborative Care
No cure for MS, care is aimed at treating the disease process and providing systematic relief
Drug Therapy: Medications used to slow the progression of MS are taken on a long-term basis
– Immunosuppressants (methotrexate), and adrenocorticotropic hormone
– Corticosteroids: used to reduce the inflammation that spikes during a relapse
– Immunomodulator (Copaxone, β-interferon): used to prevent relapses and modify progression
ADE may include flushing and SOB after injection
β-interferon (Avonex, Betaseron): rotate injection site with each dose, assess for depression and
suicidal ideation, wear sunscreen, flu-like symptoms common after initiation of therapy. Blood tests to
monitor liver enzymes.
– Gilenya: prevents lymphocytes from damaging CNS, need to have chicken pox before taking drug, monitor BP
regularly, avoid pregnancy – monitor for bradycardia
Nursing Management
During an acute exacerbation the patient may be immobile and confined to bed – prevent major complications such
as respiratory infection, UTI and pressure ulcers
Patient teaching should be focused on building general resistance to illness, including avoiding fatigue, extremes of
hot or cold
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,Musculoskeletal Disorders
Osteoporosis (fragile bone disease) calcium in bones, calcium in blood
Chronic, progressive metabolic bone disease marked by: low bone mass, deterioration of bone tissue
Leads to increased bone fragility – falls fractures
Known as “silent thief” – slowly robs you of skeletal resources
More common in women because they have lower calcium intake, less bone mass, bone resorption begins earlier
and becomes more rapid at menopause, pregnancy and breastfeeding, and live longer than men
Additional risks for fractures: smoking, low body weight, prior fractures
Risk factors: >65 yrs old, female, low body weight, family history, calcium/Vit D deficiency
Etiology and Pathophysiology
Risk factors: excessive use of alcohol (>2 a day), low testosterone in men, diet low in calcium/vitamin D deficiency,
specific diseases (malabsorption disease), certain drugs (long use of corticosteroids), thyroid replacement, heparin
Peak bone mass (by age 20) determined by heredity, nutrition, exercise and hormone function. Bone loss after 35-
40 years is inevitable
Osteoblast – bone deposit/ formation – bone building
Osteoclast – resorb bone (remodeling) – osteoclasts exceed osteoblasts in osteoporosis - breaks down bone tissue
Long term corticosteroid use is a major contributor to osteoporosis
Calcium and phosphorus abnormalities – porous brittle bones and fractures
Clinical Manifestations
Occurs in spine, hips, and wrists
First manifestations are back pain or spontaneous fractures
Gradual loss of height leading to kyphosis or “dowager’s hump”
Diagnostic Studies
Bone mineral density (BMD) – determined by peak bone mass and amount of bone loss
– Quantitative ultrasound (QUS): measures bone density with sound waves in kneecap, heel, and shin
– Dual-energy x-ray absorptiometry (DXA): measures bone density in spine, hips and forearm
T-scores
– T score above -1.0 = normal bone density
– T score between -1.0 and -2.5 = osteopenia
– T score of -2.5 or lower = osteoporosis
Z score: compares with someone own age and ethnicity: anything less than -2.0
Collaborative Care
Care focuses on proper nutrition, calcium supplementation, exercise, prevention of falls and fractures, and drugs
Proper nutrition
– 1000 mg/day of calcium in women 19-50, men 19-70 years
– 1200 mg/day of calcium for women 51+, men 71+ years
– Milk, cheese, yogurts, salmon, oysters, broccoli, almonds, turnip greens, ice cream, sardines, spinach
Calcium supplements – take in divided doses with food (easier to absorb)
– Calcium carbonate (Tums) – take with meals, 40% elemental calcium
– Calcium citrate – less dependent on stomach acid, 20% elemental calcium
– Vitamin D necessary for calcium absorption/function; bone formation. Sunlight for 20 minutes, supplemental
(800-1000IU/day) for postmenopausal, older adults, homebound, minimal sun exposure
Exercise
– Weight-bearing exercise: buildup and maintain bone mass, strength, coordination (walking, hiking)
– Walking 30 minutes, 3x a week is recommended
– Quit smoking and cur down on alcohol intake
Prevention of fractures – fall prevention
Vertebroplasty: bone cement is injected into collapsed vertebrae to stabilize, does not correct deformity
Kyphoplasty: air bladder is inserted and inflated to regain vertebral height
Drug therapy
Bisphosphonates: inhibit bone resorption
– Common side effects: anorexia, weight loss, gastritis
– Alendronate (Fosamax): once per week oral tablet
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, – Proper administration: take will full glass of water, take on empty stomach, 30 minutes before food or other
meds, remain upright for at least 30 minutes, – patient MUST be able to sit up to be a candidate for this
medication
– Prevents bone loss, bone density
– Rare/serious side effect: jaw osteonecrosis
Calcitonin: inhibits bone resorption
– Give IM form at night to minimize side effects of nausea and facial flushing
– Alternate nostrils when using nasal form – nausea does not occur with nasal spray
Teriparatide (Forteo): synthetic PTH
– Used to treat men with osteoporosis and postmenopausal women who are at risk of fractures
– First drug to stimulate new bone formation
– Side effects include leg cramps and dizziness
Denosumab (Prolia)
– Postmenopausal women, subcutaneous injection every 6 months
– For patients at high risk of fractures
Osteomalacia (Rickets)
Caused by vitamin D deficiency, resulting in decalcification and softening of bones
Softening of bone leads to gross deformities
Etiology and Pathophysiology
Lack of vitamin D: inadequate production, lack of sunlight (UV therapy), dietary deficiency, abnormal metabolism
Causes: liver disease, kidney disease, vitamin D disturbances, drug therapy (Dilantin, Fluoride, barbiturate),
malabsorption syndrome, inflammatory bowel disease
Obese patients are at risk due to inadequate calcium intake, decreased physical activity, vitamin D deficiency,
coexisting chronic conditions
Clinical Manifestations
Bone pain/tenderness, difficulty rising from chair, and difficulty walking
Muscle fatigue, weakness, weight loss, progressive deformities of spine (kyphosis) and extremities
Diagnostic Studies
Decreased serum calcium or phosphorus levels; alkaline phosphatase
X-ray: Looser’s transformation zones (ribbons of decalcification in bone found on x-ray) are diagnostic of
osteomalacia.
Collaborative Care
Aimed at correcting Vitamin D deficiency
Calcium, phosphate, and/or vitamin D supplements
Encourage dietary ingestion of eggs, meat, oily fish, and milk and breakfast cereals fortified with calcium and
vitamin D. Exposure to sunlight (and ultraviolet rays), perform weight- bearing exercise
Osteomyelitis
An infection of the bone, bone marrow, and surrounding soft tissue that results in in inflammation, necrosis, and
formation of new bone
Hematogenous osteomyelitis: due to blood borne spread of infection
– Caused by pathogens carried in the blood from other sites of infection
Contiguous-focus osteomyelitis from contamination from bone surgery, open fracture, or traumatic injury (GSW)
Osteomyelitis with vascular insufficiency, seen most commonly among patients with diabetes and peripheral
vascular disease, most commonly affecting the feet
Patients can become septic
Etiology and Pathophysiology
Exogenous: infection enters from outside as in an open fracture
Endogenous (hematogenous): organisms travel by blood from other sites of infection (bacteremia)
The pelvis, tibia, and vertebrae, which are vascular-rich sites of bone, are the most common sites of infection
Osteomyelitis may also occur in the presence of a foreign object in the body (implant, orthopedic prosthetic device
– total joint replacement)
Microorganism grows and ultimately results in ischemia and bone dies
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