priscilla diaz sanchez, m.d center for healthy aging the medical city common musculoskeletal...

Priscilla Diaz Sanchez, M.D Center for Healthy Aging The Medical City Common Musculoskeletal Diseases of Aging

Objectives Discuss the changes associated with aging in the major components of the musculoskeletal system: Bone Cartilage Skeletal muscle Others: tendons, ligaments, inter-vertebral discs Discuss the common clinical syndromes or diseases of the aging musculoskeletal system

Components of the Musculoskeletal System Bone Cartilage Skeletal muscle Others Tendons Ligaments Intervertebral discs

Aging Bones

Bone Calcium metabolism and bone metabolism interact to maintain bone integrity Calcium absorption is reduced with aging but normal serum calcium is maintained at the expense of bone volume or density Extracellular concentration of calcium is maintained by the effects of PTH, vitamin D, and calcitonin on the intestines, skeleton, and kidneys

Model of Calcium Metabolism Diet 1,200 mg Absorption Deposition 300 mg 250 mg Secretion Resorption 100 mg 250 mg Feces Reabsorption 1000 mg 8800 mg Urine 200 mg GUT ECF 900 mg Bone 0.7X 10 6 mg Glomerular Filtration 9000 mg Renal tubule

Hormones PTH Stimulation of renal tubular calcium reabsorption Stimulation of conversion of 25D to 1,25D Mobilization of calcium from bone by stimulation of osteoclastic bone resorption Vitamin D Promotes mineralization of newly formed bone Promotes intestinal calcium absorption Calcitonin Decreases bone resorption by acting directly on osteoclasts Prevents rise in serum calcium in immediate post-prandial period thereby conserving bone

Age-Related Changes in Calcium Metabolism Progressive decline in calcium absorption efficiency after the age of 70 due to: Decreased 1,25 D serum levels Decreased 1,25 D intestinal receptors Unknown age-related changes Inadequate dietary calcium intake more likely to produce negative calcium balance due to decreased efficiency of calcium absorption GFR decreases with age but no evidence for impaired renal tubular calcium handling with aging

Age-Related Changes in Calcium Metabolism Balance between bone resorption and deposition is disrupted, ranging from 0 to -30 mg/day which accumulates over time Increase in circulating levels of PTH, response to slight decrease in serum calcium Linear decrease of serum 25D levels between the ages of 65 and 90, leading to decreased 1,25 D formation Decrease in serum calcitonin which can affect balance of serum calcium levels, as calcitonin affects calcium absorption post-prandially

Bone Cortical bone changes: Reduction in thickness Increase in porosity (change in normal low surface-to-volume ratio) which leads to decreased bone strength Trabecular bone loss occurs by thinning and destruction of the entire trabeculae, a change that cannot be replaced

Bone Bone cells Osteoblasts Synthesize bone matrix Undergo either apoptosis or conversion into an osteocyte Aging: decrease in osteogenic response and an absolute decrease in the level of bone formation Produce cytokines that mediate osteoclast production: IL-1, TNFa, TGFb Osteocytes Osteoblasts that are entrapped in bone matrix Provide chemical messages that lead to increase or decrease in bone density in response to mechanical stress or microdamage Aging: increase in apoptosis of osteocytes, leading to decreased signals to form bone

Bone Bone cells continued Osteoclasts Arise from mononuclear cells and trigger bone resorption No evidence of change in function with age, but early apoptosis has been shown to limit resorptive capacity Bone remodeling Amount of bone resorbed and formed per unit of time The higher the rate of remodeling, the greater the loss of bone density Trabecular bone Resorptive phase: 30 days Bone-forming phase: 130 days plus more to become fully mineralized

Good bone Bad bone

Diseases of Aging: Bone Osteoporosis Osteomalacia Renal osteodystrophy Pagets disease of bone

Osteoporosis Disorder of bone and calcium metabolism Uncoupling of bone resorption and bone formation, normally mediated by growth factors Formation of resorptive cavity is usually followed by filling in of the cavity with new bone Formation = resorption, bone density is stable Bone resorption > bone formation, bone is lost

Osteoporosis Determinants of low bone density in women Estrogen deficiency at the menopause (type 1 or postmenopausal osteoporosis) Increased bone resorption Impaired coupling of bone formation to the increased resorption Calcium malabsorption in elderly women (type 2 or senile osteoporosis) IGF system downregulation in women over 65, with increase in IGFBP-4 which decreases bone formation Lifestyle factors, i.e. dietary calcium intake and exercise Genetic factors which determine peak bone density, reached at age 20

Osteoporosis and estrogen deficiency (Type 1 or Postmenopausal) Decreased estrogen Dec coupled bone formation Inc bone resorption ( TGFb, IGFBP-4 ) Decreased bone volume Increased serum calcium Dec PTH Inc urinary calcium Dec 1,25 D Dec calcium absorption

Osteoporosis and calcium malabsorption (Type 2 or senile) Decreased 1,25 D Local gut conditions Decreased serum calcium Decreased PTH Increased bone resorption Decreased calcium absorption Impaired coupled bone formation, IGF system Decreased bone volume

Osteoporosis and the elderly male Lower incidence of osteoporosis Peak bone density is greater in men than in women, mediated largely by testosterone Testosterone is directly anabolic to osteoblasts Decreases IL-6 production leading to decreased resorption Tendency of men to be more physically active Decline is sex hormones is more abrupt and much larger in magnitude in women than in men

Osteoporosis and the elderly male Age-dependent bone loss in males appears to be a consequence of a deficiency of estrogen as well as testosterone Testosterone deficiency leads to decreased TGFb production by bone cells which leads to poor coupling (i.e decreasing bone formation and increasing bone resorption) Other risk factors in men: decreased exercise, decreased calcium intake, and calcium malabsorption which leads to increased serum PTH levels

Bone Density in Women over time

Comparative Declines in Peak Bone Mass

Osteoporosis, clinical features Fractures Hip Vertebral Wrist Changes in body shape Kyphosis or Dowagers hump Height loss Protruding abdomen Decreased pulmonary capacity Reflux esophagitis

Osteoporosis

Osteoporotic fractures Risk factors Bone strength Trauma Risk of falling TRAUMA Force of impact FRACTURE Bone quality BONE STRENGTH Bone quantity

Clinical Factors Associated with Low Bone Density Medications: steroids, dilantin, loop diuretics, thyroid hormone, heparin, methotrexate, cylcosporin Hereditary skeletal diseases: osteogenensis imperfecta Endocrine and metabolic disorders: hyperparathyroidism, hyperthyroidism, type 1 diabetes mellitus, hypogonadism Nutritional: anorexia, malabsorption Marrow disease: myeloma, thalassemia Renal insufficency Hypercalciuria Hepatic disease Depression Spinal cord injury Systemic lupus

Osteoporosis Screening

Osteoporosis, diagnosis Radiography Bone density T-scores: standard deviations from the value at peak bone density of a young woman Osteopenia: T score less than -1 Osteoporosis: T score less than -2.5 Laboratory tests to check for secondary causes CBC, electrolytes, calcium, phosphate, creatinine, protein, liver function tests, testosterone

Osteoporosis, treatment Physical therapy Medications Estrogen/Selective Estrogen Receptor Modulators Calcium and vitamin D Bisphosphonates block osteoclastic bone resorption clinically proven to increase bone mass Calcitonin acts directly on osteoclasts alternative to women who cannot tolerate estrogens In men testosterone replacement in men who have low serum levels otherwise, bisphosphonate therapy

Osteomalacia Most commonly found in confined, dark-skinned, or diet- disbalanced individuals Primarily a defect in the mineralization of the osteoid, mainly caused by vitamin D deficiency in geriatric population Causes Insufficient sunlight Insufficient dietary vitamin D or phosphorus Renal tubular acidosis, chronic renal failure Malnutrition, malabsorption Tumor Treatment: vitamin D 10,000 IU weekly for 4-6 weeks

Renal Osteodystrophy Defective bone mineralization resulting from kidney disease Usually diagnosed with beginning treatment of end-stage kidney disease Labs: decreased calcium and calcitriol, increased phosphate and PTH Radiographs: chondrocalcinosis at knees and pubic symphysis, osteopenia, bone fractures

Renal Osteodystrophy Results from hyperparathyroidism secondary to hyperphosphatemia and hypocalcemia which are due to decreased excretion of phosphate by the kidneys Decreased renal conversion of vitamin D3 to calcitriol further contributes to hypocalcemia and hyperphosphatemia Treatment: Calcium and vitamin D supplementation, phosphate binders such as calcium carbonate, renal transplant, hemodialysis

Pagets Disease of Bone Osteitis deformans A localized disorder of accelerated bone remodeling Primary abnormality is in osteoclasts which are larger and more numerous than normal Compensatory increase in osteoblasts which leads to new bone formation which disrupts normal lamellar pattern of osteoid, forming immature woven or mosaic bone Thought to be caused by slow viruses such as paramyxoviruses Rare in people under 40 and is more common in men

Pagets Disease of Bone Increased fracture risk, deformity, and arthritis Elevated alkaline phosphatase Normal calcium, phosphate Bone scans may determine extent and activity of the disorder Radiographs: increased diameter of affected bones, particularly those of the spine or shafts of long bones Treatment: bisphosphonates, calcitonin

Other Musculoskeletal Tissues

Articular Cartilage Avascular and aneular tissue Provides smooth surface with low coefficient of friction for rapid, painless movement Synovial fluid layer provides lubrication and nutrition, the latter through motion of the joint Too thin to absorb force which is passed on to surrounding muscles and joints 70-75% water which is bound to proteoglycans to form a gel-like substance

Articular Cartilage Matrix proteins: proteoglycans called aggrecans, collagen mostly type II, glycoproteins Type II collagen: long fibrils providing tensile strength and balances osmotic pressure generated by proteoglycans Chondrocytes: control composition and organization of cartilage matrix through the synthesis and degradation of extracellular matrix components

Articular Cartilage Aging Fibrillation of cartilage surface No thinning but with reduction in cell density by 30% between ages 30 and 100 Decreased water content, probably due to changes in proteoglycan structure Stiffer collagen network due to increased cross-linking and increased fibril diameter, leading to increased proteoglycan compression Decreased collagen tensile strength Increased crystal formation and calcification

Skeletal Muscle Sarcopenia Decrease in skeletal muscle mass and quality with aging Decrease in muscle contractile force Contributes to physical disability and loss of independence Risk factor for falling and subsequent fracture Largely inevitable and independent of decreases in physical activity

Skeletal Muscle Sarcopenia Neurogenic mechanisms: age-related remodeling of muscle fibers leads to net loss of fibers, where denervation outpaces reinnervation Myogenic mechanisms: contraction-induced injury, selective primary muscle fiber atrophy (type II fibers), alterations in muscle signal transduction Combination of neurogenic and myogenic factors Other possible contributory factors: oxidative DNA damage and mitochondrial DNA mutations

Tendons and Ligaments Dense connective tissue that attach muscle to bone and bone to bone respectively Tendons transmit forces of muscle contraction to bone Ligaments serve to stabilize the joint Collagen fibers are primarily type I

Tendons and Ligaments Age-related changes may contribute to decline in joint range of motion and development of injuries Amount of trauma required to produce injuries is less in older individuals, approximately 1/3 less loading required to cause ACL to fail Strength of tendons and ligaments and their insertions to bone are reduced with age Twofold decrease in strength of anterior longitudinal ligament of the spine In shoulder joint, calcification, microtears, and fibrovascular proliferation in areas where tendon attach to bone, resulting in weakened attachment, predisposing to injury Also with stiffening of collagen due to changes in cross-linking

Inter-vertebral Discs Composed primarily of collagen types I and II which impart tensile strength Contains proteoglycans which impart resiliency Aging More marked changes in inner nucleus pulposus than outer annulus Nucleus pulposus becomes fibrotic, and fissures and cracks can be seen even in young adults Decreased cellularity, probably due to changes in nutrition Decreased hydration Changes can lead to facet joint osteoarthritis

Joints Joint: organ made up of cartilage, bone, muscle, tendon, ligament, menisci, joint capsule, and synovium Joint failure: osteoarthritis

Normal Knee

Osteoarthritis Incidence and prevalence are highly associated with age Multifactorial, heterogenous disease Joints are not equally affected Characterized by changes in both cartilage and bone Fibrillation and loss of cartilage by degradation Hypertrophic changes in subchondral bone, resulting in thickening and osteophyte formation at joint margins Chondrocytes also produce more degradative enzymes which act on matrix

Osteoarthritis Goals of management Control of pain and other symptoms Minimize functional limitation and disability Symptoms Pain Usually insidious, mild to moderate, worsened by use of joint, and improves with rest Inflammation of synovial membrane, irritation of nerve endings in joint capsule, periarticular muscle spasm, periostitis, ischemia of subchondral bone and microfractures

Osteoarthritis Symptoms, continued Stiffness Morning stiffness resolves within 30 minutes of awakening gel phenomenon: stiffness after periods of rest and inactivity, also resolves in a few minutes Loss of function Reflective of ability to perform activities of daily living Buckling/instability

Osteoarthritis Signs Bony enlargement Limitation of range of motion Crepitus on motion Tenderness on pressure Pain on motion Joint effusion Malalignment and/or joint deformity

Osteoarthritis of the Knee

Osteoarthritis of the Hand

Pyramid Approach to Osteoarthritis Management Surgery NSAIDs Acetaminophen Patient education, PT/OT, Weight reduction, Exercise, Assistive devices Intraarticular steroidsTopical analgesics

Osteoarthritis Management Symptomatic, as there is no known cure yet Nonpharmacologic modalities Patient education Cognitive behavioral therapy: designed to teach patients ways of coping with pain Social support Physical therapy: quadriceps strengthening exercises; assistive devices Aerobic exercises Weight reduction

Osteoarthritis Management Nonnpharmacologic modalities, continued Others: acupuncture, pulsed electrical stimulation, spa therapy Pharmacologic modalities Analgesics Paracetamol still first drug of choice, max 4 g a day Opioids for a limited period of time Topical analgesics, either as monotherapy or in addition to drugs Capsaicin NSAIDs

Osteoarthritis Management Pharmacologic modalities, continued NSAIDs Reasonable to try this on elderly only after failure of non-pharmacologic therapy and paracetamol Indomethacin has greater toxicity and leads to greater narrowing of joint space Ibuprofen, naproxen, ketoprofen, COX-2 inhibitors Use minimum effective dose, avoid using more than one kind of NSAID simultaneously, assess benefits after a month, use intelligent non- compliance

Osteoarthritis Management Pharmacologic modalities, continued Intra-articular therapy Intra-articular steroids work for up to 4 weeks Intra-articular hyaluronic acid, weekly injections for 3 to 5 weeks; patients 60 and older with moderate to severe symptoms and functional limitation were most likely to respond to this treatment Nutriceuticals Glucosamine sulfate with chondroitin sulfate provides symptomatic relief Antioxidant supplements, vitamin E or C Vitamin D can slow down radiographic progression Surgery: tidal lavage, total joint replacement

Rheumatoid Arthritis Criteria for diagnosis includes at least 4 of the ff: Morning stiffness of more than an hour, lasting more than 6 weeks Arthritis of at least 3 areas with soft tissue swelling lasting more than 6 weeks (PIP, MCP, wrists, elbows, knees, ankles, and/or MTP) Arthritis of hand joints lasting more than 6 weeks Symmetrical arthritis in at least one are, lasting more than 6 weeks Rheumatoid nodules Serum rheumatoid factor Radiographic changes

Rheumatoid Arthritis Prognosis in patients with 30 or more joints involved, with marked loss of ability to perform activities of daily living, is comparable to that of patients with 3-vessel coronary artery disease Other factors predictive of adverse outcomes includes presence of major co-morbidity and patients socioeconomic status

Rheumatoid Arthritis of the Hand

Rheumatoid Arthritis Work-up History: assess functional capacity, cognitive status, mood, and attitude toward disease, and to pinpoint co-morbid conditions that may influence drug choices Physical examination: note coordination, balance, and pattern of walking; look for involvement of eyes, heart, lungs, spleen, peripheral nerves in addition to joints Lab: basic blood tests, include ANA,RF, radiographs of hands and feet Synovial fluid is watery, with almost always increased white cell count

Rheumatoid Arthritis Non-pharmacologic Management Rest enough to avoid fatigue Exercises for conditioning and maintaining strength and flexibility Local therapy including moist hot packs or cold following trauma Physical supports for wrists for pain control, although does not prevent deformity Patient education and psychosocial support Orthopedic surgery to repair structural damage that may lead to disability over the long term

Rheumatoid Arthritis Pharmacologic management NSAIDs Antimalarials: chloroquin, hydroxychloroquin which may lead to eye toxicity Sulfasalazine which is selectively concentrated in connective tissues and intestinal lumen Gold salts reduce inflammatory changes and inhibits destructive effects of disease on joints; extremely toxic to kidneys and platelets Corticosteroids improve symptoms and reduce rates of progression of articular change

Rheumatoid Arthritis Pharmacologic management, continued Methotrexate suppresses inflammation in majority of cases; current evidence advocates early initiation of therapy with this drug; toxic to liver, blood cells, and lungs; folic acid should be given concommitantly Cyclosporine A has immunomodulatory actions and inhibits release of cytokines which promote tissue breakdown; toxic to kidneys

Crystal Arthropathies Gout (Monosodium urate crystal deposition disease) Hyperuricemia (serum uric acid above 6.8 mg/dl) is predisposing factor Primary: inherited disorders of uric acid metabolism, idiopathic Secondary: uric acid overproduction and underexcretion due to factors such as diet, alcohol use, lead, and drugs Men have higher levels due to lower tubular urate post secretory reabsorption related to estrogen Postmenopausal women have decreased levels of uric acid clearance, so increased predisposition to hyperuricemia May lead to kidney disease and arthritis

Secondary hyperuricemia Increased uric acid production Increased de novo purine biosynthesis Increased nucleic acid turnover Chronic hemolytic anemia Lymphoproliferative disorders Myeloproliferative disorders Psoriasis

Secondary hyperuricemia Decreased renal excretion of uric acid Drugs Diuretics Ethambutol Low-dose salicylates Pyrazinamide Preeclampsia Lead nephropathy Chronic renal failure Hyperacidemia from alcoholism, ketoacidosis, lactic acidosis, starvation

Gouty Arthritis Risk factors Hyperuricemia Family history Obesity Alcohol use Occupational and environmental lead exposure Thiazide diuretic use Renal insufficiency

Gouty arthritis MSU crystals interact with resident cells in the synovium to initiate acute gouty inflammation Acute gouty arthritis Single joint involvement, classically the MTP of big toe Any joint can be involved but usually lower extremities Triggers: trauma, alcohol, surgical stress, dietary excess, medical illness, or drugs Symptom-free intervals occur Relapses eventually tend to be polyarticular and to enter chronic tophaceous stage Chronic tophaceous gout Clinically evident subcutaneous tophi containing MSU crystals occur only after 10 years or more of bouts of acute gout Tophaceous material is white and chalky

Acute Gout Involving MTP Joint

Gouty Arthritis Radiographic findings Osteopenia with progression of articular changes Osseous erosions are common, with characteristic oval, well- circumscribed bony defects surrounded by sclerotic margins Laboratory findings Crystals on needle aspiration of synovial fluid or tophi: needle or rod-shaped and negatively birefringent under polarized light Normal serum uric acid does not exclude diagnosis of gout

Gouty Arthritis Treatment Must address prompt symptomatic relief and long-term control of disease with drugs to prevent or resorb urate deposits Alcohol consumption must be severely restricted Weight should be controlled Low purine diet may decrease serum uric acid by as much as 2 mg/dl Screen for diabetes, hypertension, and hypertriglyceridemia and treat accordingly

Gouty Arthritis Acute treatment Rest Local cold therapy NSAIDs Colchicine: efficacious in acute attacks; with GI side effects, neuromyopathy, renal failure, bone marrow suppression, DIC Intra-articular steroids for mono-articular attacks; if polyarticular, oral steroid may be prescribed Long-term steroid use may lead to local or generalized tophus formation

Gouty Arthritis Long-term management Indications for urate-lowering drugs Repeated attacks of disabling gouty arthritis Presence of tophi Chronic gouty arthritis Recurrent uric acid urolithiasis Over production of uric acid Prevention or hyperuricemia and urate sludging in collecting system of a patient scheduled to receive cytotoxic agents for treatment of hematologic malignancies

Gouty Arthritis Long-term management Initiate only after acute bout has subsided because sudden changes in uric acid may cause prolonged flares Allopurinol is drug of choice for older patients who may have impaired renal function; may cause vasculitides, nephritis, and liver toxicity To prevent breakthrough attacks during treatment, low dose colchicine or an NSAID should be given parallel

Pseudogout Calcium pyrophosphate dihydrate crystal deposition disease Involves elderly patients with acute arthritis resembling gout but with CPPD crystals in the synovial fluid and articular cartilage One of the most common arthritic disorders of the elderly, seldom seen before the 5 th decade of life May be hereditary, sporadic, idiopathic, or associated with metabolic disease or trauma

Pseudogout Serum abnormalities are not present Linked with overproduction of pyrophosphate by cartilage Interact with inflammatory cells to produce inflammation Clinical features Acute arthritis: attacks are similar to gout but less painful and last longer, usually mono- or oligoarticular, most commonly the knee Chronic : still involves knee most commonly; can be mistaken for rheumatoid arthritis

Pseudogout Diagnosis Synovial fluid: crystals are weakly positive birefringent rods or small squares, but typically rhomboid Assess serum calcium, phosphorus, magnesium, alkaline phosphatase, ferritin, glucose, iron and transferrin, TSH, and uric acid Radiographs : punctate or linear calcific densities that occur in hyaline or fibrocartilaginous tissues known as chondrocalcinosis Differs from osteoarthritis in locations such as elbow, wrist or shoulder

Pseudogout Treatment Avoid joint overuse NSAIDs Colchicine, though less effective than in acute gout Synovial fluid aspiration Intra-articular steroids No proved effective agents to dissolve CPPD crystals Joint replacement in destructive disease, with symptoms resistant to drugs

Polymyalgia Rheumatica Forms part of the spectrum of giant cell arteritis and may have same cause as temporal arteritis Aching and morning stiffness in the neck, shoulders, and buttocks Presence of symptoms in two of three commonly affected areas (shoulder girdle, hip girdle, and neck) for a month or longer, with associated findings of elevated ESR above 40 or 50 mm/hr and sometimes, rapid response to low-dose oral corticosteroids Diagnosis is excluded in the presence of RA, chronic infection, polymyositis, and malignancy

Polymyalgia Rheumatica Genetic or hereditary predisposition Cell-mediated immune reaction directed at antigens at or near elastic tissue in the arterial walls Scattered vascular involvement may be present Mean age at onset is 70 years Women are affected twice as often as men Clinical features: fatigue, anorexia, weight loss, usually in good health prior to developing PR Arthralgias, myalgias, malaise, depression, aching and stiffness

Polymyalgia Rheumatica Laboratory findings Normochromic, normocytic anemia in active phase Elevated ESR Elevated CRP Negative RF, ANA EMGs usually normal Muscle biopsy often normal but sometimes with finding of atrophy from disuse Pain seems to limit function, unlike polymyositis in which muscle weakness limits movement

Polymyalgia Rheumatica Management NSAIDs if no clinical evidence exists for a diagnosis of temporal arteritis Steroids, 15 mg prednisone; response is usually dramatic and is suggestive of diagnosis Dose is tapered over on year, sometimes using NSAID concommitantly Use ESR to monitor disease activity

Other Musculoskeletal Disorders of the elderly Bursitis Bursae cushion or reduce friction at sites where muscles and tendons pass over bony prominences or where muscles or tendons glide across each other. Synovial cell-lined, fluid-filled sacs Trauma is most common cause of bursitis, including chronic direct pressure and occupational overuse syndromes Non-traumatic causes: inflammatory arthritides such as RA, gout Infection from direct transcutaneous inoculation with S. aureus most commonly

Bursitis of the Elbow

Tendinitis Tightly packed fascicles of collagen fibrils, sheathed in connective tissue Provides elasticity and strength to transmit forces of muscle to bone Tendinitis may involve any portion of the tendon, most commonly at attachment to bone (enthesis) or at musculotendon junction Most commonly due to chronic repetitive overuse, acute overload, or direct injury

Tendinitis Aging leads to increased tendon stiffness and reduced elasticity and tensile strength from increased collagen cross- linking, progressive hypovascularity, and collagen fibril disorganization May also be manifestation of systemic inflammatory disease (RA) or crystal deposition disease Produces pain which is activity-related but may be present at rest Therapy includes relative rest, anti-inflammatory drugs, and physical therapy

Adhesive Capsulitis Frozen shoulder, shoulder periarthritis or pericapsulitis Syndrome of capsular fibrosis and generalized shoulder pain with progressive restriction of active and passive motion Self-limiting but runs a prolonged course 40-70 years old, females > males Fibrosis is due to inflammatory reaction in synovium and/or capsule

Adhesive Capsulitis Shoulder pain develops insidiously over weeks to months, commonly rest and night pain exacerbated by any shoulder motion Progressive stiffness, voluntary guarding, and disuse lead to marked reduction in all movement with pain when examined Limitation of motion arises from mechanical restriction more than pain Radiographs usually negative

Adhesive Capsulitis Treatment Goal is to restore glenohumeral motion Pain control: analgesics, NSAIDs, thermal modalities, intraarticular steroids, nerve block, TENS Avoid vigorous or forceful exercise Extensive, often prolonged, rehabilitation Most patients regain functional motion Mean recovery time may be as long as 2 years

Back Pain Low back pain is the most common regional musculoskeletal complaint among adults of all ages Elderly have higher prevalence rate, less acute-onset pain, and have higher incidence of systemic and degenerative conditions responsible for symptoms, thus warranting comprehensive evaluation Rule out malignancy, infection, compression fracture, neurologic syndromes Disk disease and facet joint osteoarthritis are common radiographic findings Therapy: bed rest, controlled physical activity, analgesics, muscle relaxant, thermal modalities, antidepressants

Nocturnal Leg Cramps Common complaint in up to 70% of elderly patients Cramps are random, sudden, involuntary painful contractions of the calf and occasionally foot muscles, occurring with recumbency and often awakening the person from sleep Cause in unclear Linked with higher prevalence of peripheral vascular disease or neurologic deficits Lack of lower extremity and knee bending activity may lead to muscle and tendon shortening which may contribute to cramps

Nocturnal Leg Cramps No relation to sleep disorders Rule out PVD, neurogenic claudication, peripheral neuropathy, thyroid disease, diabetes, fluid and electrolyte abnormalities, acohol use, diuretic anc calcium channel blocker uesage Treatment Massage and stretching Drug use is reserved for those who fail exercise therapy Quinine given 200 mg at bedtime for one week only

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