Family Nurse Practitioner III 475

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

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

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

Urate lowering drugs
Category / Mode of Action / Examples
Uricostatic drugs / Decrease uric acid synthesis (inhibit xanthine oxidase) / Allopurinol
Febuxostat (Uloric)
Uricosuric drugs / Inhibit urate reabsorption in the proximal tubule / Probenecid
Sulphinpyrazone (no longer available in the U.S.)
Losartan
Fenofibrate
Uricolytic drugs / Degrade uric acid / 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

•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

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

*** The next 3 pages are from the ACR clinical practice guidelines for gout.

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

See: American College of Rheumatology website for 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

•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

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

Management

See: American College of Rheumatology website for clinical practice guidelines
See “Diagnosis and Management of Rheumatoid Arthritis” at

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

(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.
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
Hospitalizations $8.6 billion
Nursing Home care $3.9 billion
Outpatient Services $1.3 billion
300,000 hip fractures/year in US (90% have osteoporosis)
24% excess mortality in first year
50% never fully recover
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)
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

•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
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 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:
CBC, ESR
Liver function tests
Thyroid function tests
Serum levels of albumin, phosphorous, alkaline phosphate, creatinine, and calcium
Alkaline phosphatase will be increased if there is a healing fracture
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 / Osteoporosis / Osteomalacia / Hyperparathyroidism / Tumors (such as multiple myeloma)
Serum calcium / Normal / Decreased / Increased / Normal or high
Serum phosphate / Normal / Decreased / Decreased / Normal
Serum alkaline phosphate / Normal / Increased / Increased / Normal
Other / Creatinine, thyroid profile, testosterone, leutinizing hormone / 25 hydroxy vitamin D / Parathyroid hormone / CBC, ESR, urinary and serum protein electrophoresis

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:
< age 65, postmenopausal and one or more additional risk factors
All females age 65 and over regardless of risk factors
Postmenopausal women who present with fracture
Women on HRT for prolonged period
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

Bone Density Interpretation

T-score (compares patient to standard/ideal) and is expressed in standard deviation
Normal BMD is within 1 standard deviation below the young-adult mean
In osteopenia (low bone mass), BMD is between 1 and 2.5 standard deviations of the young-adult mean
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%)

•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

•Selective Estrogen Receptor Modulator