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Family Nurse Practitioner III 475
Musculoskeletal Problems
Gout
Definitions
• Primary gout: disturbance in purine metabolism causes under-excretion or overproduction of
uric acid, leading to sodium urate crystals; inherited disease
• Secondary gout: increased uric acid from myeloproliferative disease or its treatment (hemolytic
anemia, renal disease, psoriasis, use of diuretics, etc.)
Risk Factors
• Hyperuricemia
– under-excretion by the kidneys
– metabolic overproduction
– combination
• Male
• Alcohol abuse
• Obesity
• Age: middle-aged men and postmenopausal women
• Family history of gout
• Drugs (diuretics, low-dose salicylates, cyclosporine)
• Other: renal insufficiency, HTN, hematologic malignancy
Provocative factors that can trigger an acute gout attack
• Repetitive joint trauma
• Surgical stress
• Drugs
– diuretics in the elderly
– initiation of antihyperuricemics
• Binge on alcohol or “rich” foods
Four stages in the history of gout
• Stage I: Asymptomatic hyperuricemia
• Stage II: Acute gouty arthritis
• Stage III: Intercritical gout (the asymptomatic intervals between attacks)
• Stage IV: Chronic tophaceous gout
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Key Clinical Findings
• Key Symptom: Acute severe throbbing joint pain
• Key Signs
– warmth
– redness
– swelling
– tenderness
Diagnostic Testing for Gout
• Analysis of synovial fluid or tophaceous aspiration
• Serum uric acid
• Radiographs
• 24-hour excretion of uric acid
Differential Diagnosis
• Infection
• Rheumatoid arthritis
• Bursitis (prepatellar or olecranon)
• Acute trauma
• B27-associated diseases (Reiter’s syndrome and reactive arthritis)
Goals of Treatment
• Terminate the acute attack
• Prevent recurrent attacks
• Normalize the hyperuricemia
Terminating the Acute Attack
• Begin treatment immediately
• NSAIDs = initial drugs of choice (start with loading dose)
– Indomethacin
– Naproxen
• After attack resolves, taper medications over 24-48 hours
• Other: colchicine, corticosteroids
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Preventing Recurrent Attacks
• Avoid prophylaxis until after 2nd or 3rd acute attack
• Med options for recurrent gout:
2-3 weeks post acute episode
 Allopurinal
 Febuxostat
 Probenecid
 NSAIDs
• May d/c if attack-free for 6-12 months
Category
Uricostatic drugs
Uricosuric drugs
Uricolytic drugs
Urate lowering drugs
Mode of Action
Decrease uric acid synthesis
(inhibit xanthine oxidase)
Inhibit urate reabsorption in
the proximal tubule
Degrade uric acid
Examples
Allopurinol
Febuxostat (Uloric)
Probenecid
Sulphinpyrazone (no longer
available in the U.S.)
Losartan
Fenofibrate
Uricase
Source: Schlesinger, N. (Sept. 2009) Management of gout in seniors: Addressing barriers and setting goals for
optimal control. Supplement to Clinical Geriatrics, 8-14.
Normalizing the Hyperuricemia (Goal < 6 mg/dL)
• First treat risk factors and attempt to correct the underlying cause
• If does not work, consider pharm treatment for either:
– serum uric acid > 13 mg/dl or
– 24-hour uric acid excretion of < 1100 mg
For “Underexcreter”
• Uricosuric agent is drug of choice in patients < 60 years old, with good renal function*, and no
history of kidney stones
** Uricosuric drugs require a creatinine clearance of > 50 ml to be effective.
• Uricosuric of choice: probenecid
– safe drug
– SE: skin rash and GI upset
For “Overproducer” & “Underexcreter”
Allopurinol - decreases uric acid production
• Used in those who do not meet requirements for probenecid
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No need to check 24-hour uric acid excretion
SE can be severe: GI upset, HA, rash, marrow suppression, fever, liver or kidney failure,
vasculitis, alopecia, lymphadenopathy
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Typical Stepwise Therapy:
 Single agent XOI (xanthine oxidase inhibitor) titrated to maximum appropriate dose.
 If serum urate target not achieved and there is continuing disease activity, add uricosuric
to XOI with both agents titrated to maximum appropriate dose
 If serum urate target not achieved, and there is continuing disease activity, add
pegloticase (Uricase)
Diet/Activity/Education
• Diet
– modify dietary and alcohol-use patterns
– purine restriction difficult to follow/uncertain benefit
• Activity: limit stress on the joints
• Patient Education:
– Gout is a “symptom” of the disease hyperuricemia
Follow-Up
• F/U in 1-2 weeks after acute attack to:
– review therapy, lab results, and medication side effects; to plan antihyperuricemic therapy
• See again in 4-6 weeks
– to adjust meds and review treatment goals
• If well-managed, follow yearly
• * Start preventive therapy 1 month after resolution of acute attack, if appropriate.
See: American College of Rheumatology website for clinical practice guidelines
http://www.rheumatology.org/Practice/Clinical/Guidelines/Clinical_Practice_Guidelines/
*** The next 3 pages are from the ACR clinical practice guidelines for gout.
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Osteoarthritis
Definition
 Noninflammatory arthritis in which there is deterioration of the articular cartilage and
bony overgrowth of the joint surface
 Also called degenerative arthritis, degenerative joint disease
Patient Profile
• Males = Females
• Most common age > 40 years
• Risk factors
– past joint trauma
– obesity
– normal aging process
– occupational overuse
Signs and Symptoms
• Dull, aching joint pain, tenderness
• Decreased ROM in joint
• Joint enlargement
– Heberden’s nodes (DIPs)
– Bouchard’s nodes (PIPs)
• Joint crepitus
• Joint stiffness (occurs with rest, improves with activity)
Differential Diagnosis
• Osteoporosis
• Malignancy
• Tendinitis
• Bursitis
• Vasculitis
• RA
• Gout
• Pseudogout
Workup
• Laboratory: only needed to rule out other causes
• Radiology: Plain films of affected joint(s):
– narrowed joint space, bone cysts, osteophytes
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See: American College of Rheumatology website for clinical practice guidelines
http://www.rheumatology.org/Practice/Clinical/Guidelines/Clinical_Practice_Guidelines/
for use of nonpharmacologic and pharmacologic therapies in osteoarthritis of the hand, hip, and
knee.
Treatment
• Weight loss
• Exercise program
• Warm, moist heat may be beneficial
• Pain control (biofeedback, relaxation, meditation)
• Meds: acetaminophen, ASA, oral NSAIDs, capsaicin analgesic lotion (for hands), topical
NSAIDs, tramadol
• Recommend that persons age 75+ years should use topical rather than oral NSAIDs.
Follow-Up
• Every 2 weeks X 2
• If stable, every 3-6 months
– monitor for medication side effects, such as peptic ulcer
• May need joint replacements in future
Rheumatoid Arthritis (RA)
Definition
A chronic inflammatory disease that predominantly affects the peripheral joints
Etiology of RA
• Unknown
• Genetic predisposition appears to be important
• Most commonly believed etiology: autoimmunity
• Cellular and immune mechanisms result in destructive inflammatory process, primarily
involving the synovium.
Course of RA
• Affects women 3X more commonly than men
• Most common age: 25-45 years
• Begins insidiously in most cases
• Usually progressive but often with exacerbations and remissions
Signs & Symptoms of RA
• Insidious onset: fatigue, anorexia, weight loss, generalized stiffness
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Proceeds to symmetric joint swelling and warmth of hands, feet, wrists, knees, hips
PIPs, MCP, and wrist joints typically involved
Also MTP, ankle, knee, elbow jts., C-spine
DIPs, thoracic/lumbar spine typically spared
Joint stiffness after waking and after periods of inactivity
Deformities due to inflammation and fibrosis of joint capsule (ulnar drift, swan neck,
boutonniere deformity)
Rheumatoid nodules
Lymphadenopathy; splenomegaly
Ocular disease
Work-Up
• CBC: mild anemia (of chronic disease)
• ESR: usually elevated
• Rheumatoid Factor > 1:80 titer (80% of pts)
• Positive ANA in 30% of RA patients
• Synovial fluid: decreased viscosity, and increased WBC count
Differential Diagnosis
• Systemic lupus erythematosus
• Osteoarthritis
• Polymyositis
• Gout
• Pseudogout
• Scleroderma
• Chronic infection
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Rheumatoid Arthritis Criteria (1987 Revision--American Rheumatism Association)
Copyright © 2000, L. Leff, MD
Morning stiffness
Morning stiffness in and around the joints, lasting at least 1 hour before maximal
improvement. (1 point )
Arthritis of 3 or more joint areas
At least 3 joint areas simultaneously have had soft tissue swelling or fluid (not bony
overgrowth alone) observed by a physician; the 14 possible joint areas are right or left
proximal interphalangeal (PIP) joints, metacarpophalangeal (MCP)joints, wrist, elbow,
knee, ankle, and metatarsophalangeal (MTP) joints. (1 point )
Arthritis of hand joints
At least one area swollen (as defined above) in a wrist, MCP or PIP joint. (1 point)
Symmetric arthritis
Simultaneous involvement of the same joint areas (see 2 above) on both sides of the body
(bilateral involvement of PIPs, MCPs, or MTPs is acceptable without absolute
symmetry). (1 point )
Rheumatoid nodules
Subcutaneous nodules, over bony prominences, or extensor surfaces, or in juxta-articular
regions, observed by a physician. (1 point )
Serum rheumatoid factor
Demonstration of abnormal amounts of serum rheumatoid factor by any method for
which the result has been positive in < 5% of normal control subjects. (1 point)
Radiographic changes
Radiographic changes typical of RA on posteroanterior hand and wrist radiographs,
which must include erosions or unequivocal bony decalcification localized to or most
marked adjacent to the involved joints (osteoarthritis changes alone do not qualify). (1
point )
* For classification purposes, a patient shall be said to have rheumatoid arthritis if he/she has
satisfied at least 4 of these 7 criteria. Criteria 1 through 4 must have been present for at least 6
weeks.
Total Criteria Point Count: ____________
RA Score:
4-7 points = Diagnostic of Rheumatoid Arthritis
2-3 points = Cannot exclude RA
0-2 points = Unlikely RA
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Management
 See: American College of Rheumatology website for clinical practice guidelines
http://www.rheumatology.org/Practice/Clinical/Guidelines/Clinical_Practice_Guidelines/
 See “Diagnosis and Management of Rheumatoid Arthritis” at
http://www.aafp.org/afp/2011/1201/p1245.pdf
Interventions: Patient Education
• Importance of good nutrition
• Moderate exercise program
• Avoid heavy work and vigorous exercise
• Living with a chronic illness
• Splints to help avoid deformity
• Warm, moist heat for relief of stiffness
• Ice packs during active periods
Referrals and Follow-Up
• F/U in 2 weeks X2, then monthly X 2, then every 3 months
• Referrals to:
– rheumatologist, if available
– physical therapist
– occupational therapist
RA can be a devastating disease.
The patient needs a great deal of psychologic support and encouragement.
Osteoporosis
Review National Osteoporosis Foundation’s Clinical Guide to Prevention and Treatment of
Osteoporosis at http://nof.org/hcp/clinicians-guide (and also available as an app for a small
fee)
Definition
A loss of bone mass that increases susceptibility to fracture. Bone loss occurs when the rate of
reabsorption is greater than the rate of formation.
Demographics
 Although osteoporosis has been considered a disease of women, its existence in men has
been well documented by epidemiological studies.
o Of the 10 million Americans who have osteoporosis, 2 million are men and an
additional 3.5 million men are at risk for the disease
 Medical cost of fractures in US = $13.8 billion
o Hospitalizations $8.6 billion
o Nursing Home care $3.9 billion
o Outpatient Services $1.3 billion
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300,000 hip fractures/year in US (90% have osteoporosis)
o 24% excess mortality in first year
o 50% never fully recover
o 25% require LTC/Nursing Home care
Although hip fracture incidence is lower in men than in women, 36% of men die the year
following a fracture, nearly twice the percentage of women.
Once person has 1 vertebral fracture, very high risk of more fractures (vertebral, hip)
For 50 year old female, there is a 40% risk of having an osteoporotic fracture in her
remaining lifetime
The age of men with primary osteoporosis varies from 23 to 86 years although the average
age is in the mid-60s.
Osteoporosis occurring in either sex after age 70 is classified as senile.
Causes of Bone Loss in Women
 Estrogen deficiency—causes 15% of bone loss (first phase—postmenopause)
o Note: Effect of hormone therapy is erased after being off estrogen for 7 years
 Disuse—causes 6% of bone loss
 Calcium and Vitamin D deficiency—causes 16% of bone loss (occurs mainly 15-20 years
after menopause)
Primary Osteoporosis in Women
• Type I: postmenopausal endocrine changes; imbalance between bone formation and
resorption (due to decreased estrogen)
– usually affects women 15-20 years after menopause
– rate of trabecular bone loss is markedly increased
– predisposes vertebral bodies and radius to fractures
• Type II: age-related reduction in vitamin D
– affects men and women 70 + years old
– usually hip and vertebral fractures
– proportionate loss of trabecular and cortical bone
Causes of Secondary Osteoporosis in Women
• Hyperthyroidism
• Hyperparathyroidism
• Hypogonadism
• Hyperprolactinism
• DM
• Corticosteroids
• Ethanol
• Tobacco
• Barbiturates
• Chronic renal failure
• Liver disease
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COPD
RA
Malignancy
Cushing’s syndrome
Risk Factors Associated with Osteoporosis in Women
• Age older than 65
• Female gender
• Caucasian or Asian race
• Thin body frame
• Family history (ask if patient mother ever broke her hip…increases risk!)
• Longstanding Ca def.
• Underweight (obesity is protective)
• Sedentary lifestyle
• Use of thyroid replacement therapy, steroids, or heparin
• Alcohol abuse (alcohol can be toxic to cells in bone marrow)
• Cigarette smoking (reduces ambient estrogen level)
• Renal/liver disease
• Secondary amenorrhea
• Multiple myeloma
• Endocrine disease
Classifications of Osteoporosis in Men
 Primary: unknown cause
 Secondary: caused by alcoholism, anticonvulsants, GI disorders, glucocorticoid excess,
hypercalciuria, hypogonadism, immobilization, long-term heparin or warfarin therapy,
neoplastic diseases, organ transplantation, rheumatoid arthritis, smoking, and thyrotoxicosis
 Senile: caused by alteration in calcium homeostasis, inadequate calcium and vitamin D
intake, and physical inactivity
Risk Factors for Osteoporosis in Men
 Hereditary: Family history of osteoporosis, advanced age, thin build, Caucasian or Asian
race
 Lifestyle: Physical inactivity, smoking, excessive alcohol use, weight loss
 Dietary: Insufficient calcium and vitamin D, excessive sodium, excessive protein, excessive
caffeine
 Medical: Absent or low testosterone levels; androgen-deprivation therapy; cancer; growth
hormone deficiency; overactive thyroid, parathyroid, or adrenal glands; chronic intestinal
diseases; organ transplantation
o Testosterone has a major impact on the attainment of peak BMD and the
maintenance of BMD in men. Although an abrupt cessation of testicular function
does not occur, total and free testosterone levels may decline with age or remain in
the normal range into the ninth decade. Elderly men with low testosterone levels are
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more than twice as likely to have hip fractures than men of similar age with normal
testosterone levels.
Pharmacologic: Vitamin D overdose, vitamin A overdose, corticosteroids (oral, inhaled,
nasal), chemotherapy drugs, long-term heparin or warfarin therapy, aluminum-containing
antacids
Symptoms
• Result from fractures of vertebrae, wrist, hip, humerus
• Generalized skeletal pain is uncommon
• Pain usually results from collapse of the vertebrae, often with minimal trauma
• Hip fractures from moderate trauma
– impaired ability to walk
• Distal forearm fx: tries to break a fall
Work-Up
 Tests to R/O secondary osteoporosis:
o CBC, ESR
o Liver function tests
o Thyroid function tests
o Serum levels of albumin, phosphorous, alkaline phosphate, creatinine, and calcium
 Alkaline phosphatase will be increased if there is a healing fracture
o Serum levels of testosterone and luteinizing hormone (LH) should be included
because of the clear association of hypogonadism and osteoporosis in men
 The total testosterone level, which measures bound and free testosterone in the
serum, is the preferred test.
 Testosterone levels normally undergo rapid diurnal changes; they are highest
in the morning and drop by 30-50% in mid-afternoon
Differential Diagnosis of Osteoporosis [From: Lawson, M.J. (2001). Evaluating and managing
osteoporosis in men. In CE Connection: Advanced Pharmacology, 44-55.]
Laboratory
Test
Serum calcium
Serum
phosphate
Serum alkaline
phosphate
Other
Osteoporosis
Osteomalacia
Hyperparathyroidism
Normal
Normal
Decreased
Decreased
Increased
Decreased
Tumors (such
as multiple
myeloma)
Normal or high
Normal
Normal
Increased
Increased
Normal
Creatinine,
thyroid profile,
testosterone,
leutinizing
hormone
25 hydroxy
vitamin D
Parathyroid hormone
CBC, ESR,
urinary and
serum protein
electrophoresis
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Bone mineral density measurements (BMD)
• Helpful in diagnosis and prevention of osteoporosis
• Measurements are different at various skeletal sites due to differing amounts of cortical and
trabecular bone
• Several techniques for measurement of bone mass: SPA, DPA, QCT, DEXA
 Test if:
o < age 65, postmenopausal and one or more additional risk factors
o All females age 65 and over regardless of risk factors
o Postmenopausal women who present with fracture
o Women on HRT for prolonged period
o Women considering therapy for osteoporosis if BMD testing would facilitate the
decision (to get baseline – F/U DEXA in 2-3 years)
DEXA
• = dual energy x-ray absorptiometry
• “Gold standard”
• Can measure density at spine, hip, wrist, total skeleton
• Accurate and precise
• Exam time low: 10 minutes
• Radiation low: 1-3 mrems
SPA
• = Single-photon absorptiometry
• Measures density of appendicular bone (radius, calcaneus)
• Exam time short: 10-20 minutes
• Radiation exposure = 5 mrem
QCT
• = quantitative computed tomography
• Used mostly for spinal area, but also hip and radius
 Allows assessmento f trabecular bone alone
• Exam time short: 10-20 minutes
• Significantly more radiation exposure
– (> 200 mrem)
• Less accurate than other techniques, expensive
Ultrasonometry
 Site: heel, fingers, tibia
 Inexpensive, portable, no radiation
 Less precise
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Bone Density Interpretation
 T-score (compares patient to standard/ideal) and is expressed in standard deviation
o Normal BMD is within 1 standard deviation below the young-adult mean
o In osteopenia (low bone mass), BMD is between 1 and 2.5 standard deviations of the
young-adult mean
o Osteoporosis is defined as a BMD of 2.5 or greater standard deviations below the
young-adult mean
 Z-score (compares to own age group)
Use of FRAX (Fracture Risk Assessment Tool
Prevention of Osteoporosis
• Maximization of peak bone mass
– adequate calcium and vitamin d intake
– avoidance of smoking and heavy alcohol use
– regular exercise
• Minimizing bone loss from menopause
– Estrogen replacement therapy
– 1000-1500 mg of calcium; adequate vitamin D
– encourage weight-bearing exercise
Treatment of Established Osteoporosis
• 1200-1500 mg calcium (carbonate or citrate)/400-800 IU vitamin D3 (*** calcium
supplementation of 500 mg or more per day without Vitamin D increases the risk of MI by
30%)
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Calcium Metabolism Modifiers
• Calcitonin [Miacalcin] (50 U/day) if unwilling or unable to take estrogen or for men
[used for treatment only]
• Bisphosphonate: inhibit osteoclast bone resorption [used for prevention and treatment]
• Alendronate (Fosamax)
• Risedronate (Actonel)
• Ibandronate (Boniva)
• Reclast (zoledronic acid) also a bisphosphonate; 5 mg IV q 12 months. Hydrate patient
prior to administration. Cost: (Epocrates): $1137.
Parathyroid Hormone Analogues
Forteo (teriparatide) regulates bone metabolism, intestinal calcium absorption, and renal
tubular calcium and phosphate reabsorption; given 20 mcg subcu q day
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Selective Estrogen Receptor Modulator
• Evista (raloxifene) (selective estrogen receptor modulator) selectively binds to estrogen
receptors, inhibiting bone resorption and turnover [used for prevention]
Monoclonal Antibodies, Endocrine
Prolia (denosumab) first of a new class of agent; should be considered a second-line
treatment; a fully human monoclonal antibody to RANKL
o Denosumab binds to the receptor activator of nuclear factor-kappa B ligand
(RANKL), a soluble protein/cytokine essential for the formation, function, and
survival of osteoclasts, which are the cells responsible for bone resorption.
o Given 60 mg subcu every 6 months
NSAIDs or other analgesics for pain
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QUESTION: Are there any concerns/problems with using bisphosphanates?
QUESTION: How long do you treat osteoporosis with pharmacologic agents?
Treatment Algorithm for Osteoporosis
 If known to have vertebral fracture: treat with bisphosphonate, calcitonin, Forteo (depending
on severity and patient)
 If no known vertebral fracture:
o If not willing to consider pharmacological treatment, treat with OTC calcium with
vitamin D, exercise, and no smoking
o If willing to consider treatment:
 If > 65 years old, get BMD measurement
 If < 65 years old
 If no risk factors, treat with OTC calcium, exercise, no smoking. Offer
BMD measurement
 If risk factors present, get BMD measurement
Falls in the Older Adult
Source: Moncada, LVV. (Dec. 1, 2011) Management of falls in older persons: A prescription for prevention.
American Family Physician, 84 (11), 1267-1276.
Nonmodifiable Risk Factors for Falls in Older Adults
 Age older than 80 years
 Arthritis
 Cognitive impairment/dementia
 Female sex
 History of CVA or TIA
 History of falls
 History of fractures
 Recently discharged from hospital (within 1 month)
 White race
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Potentially Modifiable Risk Factors for Falls in Older Adults
 Environmental hazards
 Medications
o Antidepressants (tricyclics, SSRIs)
o Antihypertensives
o Antipsychotics
o Benzidiazepines
o Diuretics
o NSAIDs
o Sedatives and hypnotics
o Polypharmacy (4+ prescription medications)
 Metabolic factors
o Dehydration
o Diabetes
o Low BMI
o Vitamin D deficiency
 Musculoskeletal factors
o Balance impairment
o Foot problems
o Gait impairment
o Impaired ADLs
o Lower extremity muscle weakness
o MSK pain
o Use of assistive device
 Neuropsychologic factors
o Delirium
o Depression
o Dizziness or vertigo
o Fear of falling
o Parkinson disease
o Peripheral neuropathy
 Sensory impairment
o Auditory impairment
o Multifocal lens use
o Visual impairment
 Other
o Acute illness
o Alcohol intoxication
o Anemia
o Cardiac arrhythmia
o Inappropriate footwear
o Obstructive sleep apnea
o Orthostatic hypotension
o Urinary incontinence
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Review: 2010 AGS/BGS Clinical Guidelines at
http://www.guideline.gov/content.aspx?id=37707
Note: You can download the AGS app for a small fee!
Fibromyalgia Syndrome (FMS)
Source: Buttaro, TM, Trybulski, J, Bailey, PP, & Sandberg-Cook, J. (2008) Primary care: A collaborative practice
(3rd ed.). St. Louis: Mosby Elsevier.
Definition
 A disorder characterized by symptoms of widespread musculoskeletal pain, fatigue, nonrestorative sleep, depression, headaches, and GI complaints such as IBS
 Defined as > 3 months of musculoskeletal pain present above and below the wait
bilaterally, associated with pain on palpation of tender points, with no other source of
pain identified. The pain is usually accompanied by profound fatigue and sleep
disturbance
 May occur in presence of other rheumatologic disorders such as SLE and RA
 Most patients with chronic fatigue syndrome also meet the diagnostic criteria for FMS
Demographics
 8-9 X more prevalent in women than men
 Onset generally at 40-50 years of age; rarely begins after age 55
 Approx. 2% of total population is affected, with incidence increasing with age to 8% in
women 60-69 years old
 Affects 3-6 million Americans
 FM undiagnosed in as many as 3 out of 4 people
Pathophysiology
 New research has implicated CNS dysfunction, rather than muscle, autoimmune, or viral
disease.
 Normally pain beginning in the periphery is processed in the spinal cord and transmitted
to the brain
 In FMS, some pain becomes heard "louder" at the level of the spinal cord and brain (=
central sensitization)
 The brain responds with pain recognition at a lower threshold and over a wider area than
that originally involved.
 The cause of the CNS dysfunction is unknown at this time.
Clinical Presentation
Triad of core symptoms of FM:
 Persistent widespread pain
 chronic fatigue
 sleep disturbance (nonrestorative sleep)
Note: There is controversy as to whether chronic fatigue syndrome (CFS) and fibromyalgia are
the same or different conditions. It is suggested that they are similar with pain being the
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predominant problem in people with FM, whereas fatigue is the major complaint in people with
CFS.
Additional symptoms:
 cognitive difficulties
 allergies
 migraines
 palpitations
 IBS
 mood disorders
Physical Examination
Normal muscle strength
American College of Rheumatology 1990 Criteria for Classification of Fibromyalgia
[Patient is considered to have FM if both criteria are satisfied. The widespread pain must have
been present for >3 months]
History of widespread pain
Pain considered widespread when all of the following are present:
 pain on the left side of the body
 pain on the right side of the body
 pain above the waist
 pain lower the waist
 axial skeletal pain (cervical spine or anterior chest or thoracic spine or low back)
Pain in 11 of 18 tender point sites on digital palpation
Perform digital palpation with an approximately force of 4 kg. (8.8 pounds) of pressure
(achieved with the thumb, using enough pressure to blanch the thumbnail)
 Occiput: bilateral, at the suboccipital muscle insertions
 Low cervical: bilateral, at the anterior aspects of the intertransverse spaces at C5-C7
 Trapezius: bilateral, at the midpoint of the upper border
 Supraspinatus: bilateral, at origins, above the scapula spine near the medial border
 Second rib: bilateral, at the second costochondral junctions, just lateral to the junctions
on upper surfaces
 Lateral epicondyle: bilateral, 2 cm distal to the epicondyles
 Gluteal: bilateral, in upper outer quadrants of buttocks in anterior folds of muscle
 Greater trochanter: bilateral, posterior to the trochanteric prominence
 Knee: bilateral, at the medial fat pad proximal to the joint line
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Diagnostics
 In-depth H & P
 Exclude underlying autoimmune disorders such as RA and lupus thru normal labs
including CBC, ESR, RF, ANA, and TSH
 Vitamin D-25-hydroxalase: low levels may worsen muscle pain and balance; treat with
high dose oral vitamin D
 Hepatitis C: symptoms of hepatitis C mimic those of FM
 Sleep studies may be done for those with obstructive sleep apnea/daytime sleepiness
(falling asleep during daytime activities such as driving)
Differential Diagnosis
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myofascial pain syndrome
chronic fatigue syndrome
hypothyroidism
bursitis/tendinitis
depression
anxiety
RA
SLE
PMR
polymyositis
Management
Goals of therapy: patient empowerment to control pain, enhance sleep, maintain mobility
Pharmacology
 amitriptyline (Elavil) 10-20 mg, taken 2-3 hours before bedtime
 cyclobenzaprine (Flexeril) 5-10 mg at hs
 SSRIs (such as Prozac) alone or in combination with amitriptyline
 dufloxatine (Cymbalta), a dual serotonin-norepinephrine reuptake inhibitor
 gabapentin (Neurontin) 300 mg tid
 pregabalin (Lyrica)
 Trazodone (Desyrel) and zolpidem (Ambien) may help sleep
Cognitive Behavioral Therapy
 coping skills
 relaxation training
 activity pacing
 visual imagery techniques
 goal setting
Exercise
 gentle stretching before exercise
 aerobic exercise
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Complications
 disability
 depression
 insomnia
 muscle atrophy
 misdiagnosis
 drug-seeking behavior
Polymyalgia Rheumatica
Demographics
 Average age of onset: 65-70 (rare in people under 55)
 Occurs 1:200 people > age 65
 Women affected twice as often as men
 Whites affected much more frequently than African-Americans
Cause
 Underlying cause of PMR has not been discovered (no infectious agents, no environmental
factors)
 Possible genetic factors (due to commonality in whites
 Since it is seen almost exclusively in the elderly suggests mechanisms involving senescence
of the immune system
Signs/Symptoms
 New or increased pain and stiffness of the shoulders and hips (limb-girdle muscle pain and
stiffness)
o Since more than half of the aged have documented MSK disease, it is easy to assume
that an existing process has flared up
o May be unilateral early on, but quickly become symmetrical
o Typically, low neck and proximal shoulder muscles are affected before the hip,
buttock, and thigh muscles
 Patients often restrict activity because of pain and so suffer secondary muscle atrophy,
weakness, and growing dependence, often becoming depressed
 Associated symptoms are often revealed only by specific inquiry:
o Intermittent mild fever
o Night sweats
o Modest loss of appetite and weight
o Fatigue
o Malaise
o Depression
 PMR unrecognized in the majority of its victims
 Symptoms may emerge rapidly, but more typically the presentation is insidious, with
graduate progression of proximal muscle pain and stiffness over several weeks
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
The course of the disease, if not treated, is chronic and steady over months to years, after
which symptoms may remit. However, flare-ups may occur years after the original episode.
Diagnosis
 Based on the clinical picture
 ESR > 40, and often > 100, is typical and may be used to monitor the response to therapy
 Normochromic anemia, as seen in other chronic inflammatory diseases, is typical
 WBC and differential typically normal
 ANA and RF tests and CPK normal
Treatment
 Oral low-dose steroids, starting with 15-20 mg of prednisone daily
 If the symptoms resolve and the ESR returns to essentially normal within a month, the dose
may be tapered slowly
 The daily maintenance dose may be as low as 5 mg, but if symptoms or elevated ESR return,
higher doses must be given
 Prednisone is usually maintained for at least a year and may be needed must longer before
being successfully tapered and stopped.
Disease Progression/Remission/Complication
 More than 2/3 of patients achieve full remission or long symptom-free periods without
prednisone.
 However, relapses are common and can be seen as late as 8 years after successful treatment
 Giant cell arteritis may be seen at some time in as many as 1/3 of patients with PMR (to be
discussed in Neuro section)