Priscilla Diaz Sanchez, M.D Center for Healthy Aging The Medical City Common Musculoskeletal...
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- Slide 1
- Priscilla Diaz Sanchez, M.D Center for Healthy Aging The
Medical City Common Musculoskeletal Diseases of Aging
- Slide 2
- 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
- Slide 3
- Components of the Musculoskeletal System Bone Cartilage
Skeletal muscle Others Tendons Ligaments Intervertebral discs
- Slide 4
- Aging Bones
- Slide 5
- 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
- Slide 6
- 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
- Slide 7
- 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
- Slide 8
- 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
- Slide 9
- 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
- Slide 10
- 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
- Slide 11
- 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
- Slide 12
- 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
- Slide 13
- Slide 14
- Good bone Bad bone
- Slide 15
- Diseases of Aging: Bone Osteoporosis Osteomalacia Renal
osteodystrophy Pagets disease of bone
- Slide 16
- 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
- Slide 17
- Osteoporosis Determinants of low bone density in women Estrogen
deficiency at the menopause (type 1 or post- menopausal
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
- Slide 18
- 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
- Slide 19
- 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
- Slide 20
- 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
- Slide 21
- 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
- Slide 22
- Bone Density in Women over time
- Slide 23
- Comparative Declines in Peak Bone Mass
- Slide 24
- Osteoporosis, clinical features Fractures Hip Vertebral Wrist
Changes in body shape Kyphosis or Dowagers hump Height loss
Protruding abdomen Decreased pulmonary capacity Reflux
esophagitis
- Slide 25
- Osteoporosis
- Slide 26
- Osteoporotic fractures Risk factors Bone strength Trauma Risk
of falling TRAUMA Force of impact FRACTURE Bone quality BONE
STRENGTH Bone quantity
- Slide 27
- 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
- Slide 28
- Osteoporosis Screening
- Slide 29
- 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
- Slide 30
- 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
- Slide 31
- 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
- Slide 32
- 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
- Slide 33
- 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
- Slide 34
- 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
- Slide 35
- 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
- Slide 36
- Other Musculoskeletal Tissues
- Slide 37
- 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
- Slide 38
- 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
- Slide 39
- 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
- Slide 40
- 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
- Slide 41
- 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
- Slide 42
- 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
- Slide 43
- 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
- Slide 44
- 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
- Slide 45
- Joints Joint: organ made up of cartilage, bone, muscle, tendon,
ligament, menisci, joint capsule, and synovium Joint failure:
osteoarthritis
- Slide 46
- Normal Knee
- Slide 47
- 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
- Slide 48
- 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
- Slide 49
- 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
- Slide 50
- 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
- Slide 51
- Osteoarthritis of the Knee
- Slide 52
- Osteoarthritis of the Hand
- Slide 53
- Pyramid Approach to Osteoarthritis Management Surgery NSAIDs
Acetaminophen Patient education, PT/OT, Weight reduction, Exercise,
Assistive devices Intraarticular steroidsTopical analgesics
- Slide 54
- 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
- Slide 55
- 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
- Slide 56
- 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
- Slide 57
- 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
- Slide 58
- 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
- Slide 59
- 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
- Slide 60
- Rheumatoid Arthritis of the Hand
- Slide 61
- 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
- Slide 62
- 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
- Slide 63
- 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
- Slide 64
- 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
- Slide 65
- 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
- Slide 66
- Secondary hyperuricemia Increased uric acid production
Increased de novo purine biosynthesis Increased nucleic acid
turnover Chronic hemolytic anemia Lymphoproliferative disorders
Myeloproliferative disorders Psoriasis
- Slide 67
- 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
- Slide 68
- Gouty Arthritis Risk factors Hyperuricemia Family history
Obesity Alcohol use Occupational and environmental lead exposure
Thiazide diuretic use Renal insufficiency
- Slide 69
- 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
- Slide 70
- Acute Gout Involving MTP Joint
- Slide 71
- 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
- Slide 72
- 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
- Slide 73
- 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
- Slide 74
- 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
- Slide 75
- 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
- Slide 76
- 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
- Slide 77
- 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
- Slide 78
- 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
- Slide 79
- 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
- Slide 80
- 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
- Slide 81
- 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
- Slide 82
- 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
- Slide 83
- 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
- Slide 84
- 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
- Slide 85
- Bursitis of the Elbow
- Slide 86
- 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
- Slide 87
- 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
- Slide 88
- 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
- Slide 89
- 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
- Slide 90
- 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
- Slide 91
- 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
- Slide 92
- 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
- Slide 93
- 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
- Slide 94