Download Chapter 12 Musculoskeletal Function

Chapter 12
Musculoskeletal
Function
Musculoskeletal System
• Includes bones, joints, muscles,
ligaments, tendons, and other
connective tissue
• Purpose:
– Support for the body
– Protection of organs
– Stores calcium and other minerals
– Site for hematopoiesis
Bones
• Specialized form of connective tissue
• Site of fat and mineral storage as well as
hematopoiesis
• 206 bones in the skeleton
• Skeletal divisions
– Axial skeleton forms the long axis of the body
and includes the skull, vertebral column, and rib
cage
– Appendicular skeleton consists of bones that
form the arms, shoulders, pelvis, and legs
Types of Bones
• Long bones
– Length is greater than width
– Growth plates are at either end
– Outer surfaces are hard (compact bone)
– Inner regions are less dense (spongy bone)
– Contain bone marrow
– Include some of the longest bones in the body
(e.g., femur, humerus, and tibia) and some of the
smallest (e.g., metacarpals, metatarsals, and
phalanges)
Types of Bones
• Short bones
– Are approximately as wide as they are long
– They provide support and stability with little
movement
– Contain a thin layer of compact bone along with
spongy bone and relatively large amounts of
bone marrow
– Include the carpals and tarsals
Types of Bones
• Flat bones
– Strong, level plates of bone
– Provide protection to the body’s vital organs and
a base for muscular attachment
– Anterior and posterior surfaces form from
compact bone to provide strength
– Center consists of spongy bone and varying
amounts of bone marrow
– In adults, most red blood cells are formed here
– Include the scapula, sternum, skull, pelvis, and
ribs
Types of Bones
• Irregular bones
– Do not fall into any other category due to their
nonuniform shape
– Primarily consist of spongy bone, with a thin
outer layer of compact bone
– Include the vertebrae, sacrum, and mandible
Types of Bones
• Sesamoid bones
– Usually short or irregular bones embedded in a
tendon
– Often present in a tendon where it passes over a
joint and serves to protect the tendon
– Include the patella, pisiform (smallest of the
carpals), and the two small bones at the base of
the first metatarsal
Bones
• Periosteum – layer of connective tissue
that covers compact bone surfaces
– Serves as the site of muscle attachment (via
tendons)
– The outer surface contains cells that aid in
remodeling and repair (osteoblasts)
– Richly supplied with blood vessels and nerve
fibers
Bones
• Bone marrow – in the shaft of long bones
– Most infants have red marrow
– Red marrow is the site of hematopoiesis
– Red marrow is slowly replaced by fat with age,
creating yellow marrow
– Yellow marrow begins to form during adolescence
and is present in most bones by adulthood
– Hematopoiesis occurs in the vertebrae, pelvis,
and a few other sites in adults
– The yellow marrow can be reactivated to produce
blood cells when needed (e.g., after an injury)
Bone Remodeling
• Osteoclasts – break down spongy bone
• Osteoblasts – rebuild new compact bone
• Osteocyte – osteoblasts surrounded by calcified
extracellular material
• Lamellae - thin layers of osteocytes
• Matrix
– Extracellular material in which the osteocytes are embedded
– Consists of calcium phosphate crystals that make bones hard and
strong
– Also contains collagen fibers that reinforce the bone to give flexible
strength
– Balance between the mineral and collagen is necessary for optimal
bone function
Bone Growth
• Bones grow in two ways
– Appositional growth – new bone forms on the
surface of a bone
– Endochondral growth – bone eventually
replaces new cartilage growth in the epiphyseal
plate
• Proper nutrition and physical activity
are essential for the development and
maintenance of healthy bone
Bone Growth
• Growth hormone works with thyroid hormones to control
normal bone growth
– Causes cartilage and bone cells to reproduce and lay
down their intercellular matrix
– Stimulating mineralization within the matrix
• Calcitonin and parathyroid hormone regulate bone
remodeling and mineralization of calcium
• Estrogen inhibits formation of osteoclasts in women
• Testosterone increases bone length and density in men
• Vitamin D controls the absorption of calcium from the
intestine and increases calcium and phosphate
reabsorption in the kidneys
Bones
• The skeleton forms from hyaline cartilage
during fetal development
• Cartilage – tough and flexible connective
tissue
Joints
• Structures that connect bones of the skeleton
• Synovial joints
– Most common type
– Freely moveable
– Contain cartilage that is lubricated by a transparent
viscous fluid (synovial fluid) that contains
leukocytes to fight infections and provides nutrients
– Contains a joint capsule, a structure that joins one
bone to another
– Consists of dense connective tissue that attaches
to the periosteum of adjacent bones
– Many contain ligaments that connect bones to
bones and provide support to the joint
Joints
• Amphiarthroses joints
– Slightly moveable
– Found in the vertebral column
• Synarthroses joints
– Immoveable
– Found in the skull and pubic symphysis
Muscles
• Skeletal muscles – voluntary muscles that connect
to bone
– 350 skeletal muscles that are controlled by the brain
• Smooth muscles – involuntary muscles that line
walls of hollow organs and tubes and are found in
the eyes, skin, and glands
• Cardiac muscle – involuntary muscle that
comprises the heart
• Tendons – tough bands of dense connective tissue
that are continuous extensions of the periosteum
– Attaches muscles to bones
Skeletal Muscles
• Comprised of muscle fibers, connective tissue, blood
vessels, and nerves
• Muscle fiber – muscle cell
• Myofibrils – threadlike structures that extend the entire
length of the muscle fiber
• Myofibrils contain two types of myofilaments – actin and
myosin
• Myofilaments are organized into repeated structural units
called sarcomeres
• Muscle fibers contract by sliding actin filaments over
myosin filaments
• Calcium and adenosine triphosphate is required for
muscle contractions
Skeletal Muscles
• Sarcolemma – cell membrane that encloses
each muscle fiber
• Endomysium – connective tissue that
surrounds several muscle fibers bundled
together
• Perimysium - connective tissue that
surrounds several of bundles to form a
muscle
• Fascia - connective tissue surround the
muscle and muscle groups
Skeletal Muscle Growth
• Growth hormone causes muscle growth
• The number of muscle fibers in a muscle remains
relatively constant throughout the life span
• Increases in muscle sizes reflect increases in
individual muscle fibers
• When muscles work harder, they respond by
becoming larger and stronger from an increase in
contractile protein inside the muscle fiber
• The muscle protein is produced and destroyed
quickly, and the growth may be short lived
Understanding Musculoskeletal
Conditions
• Alterations may result in:
– Impaired Physical Mobility
– Chronic Pain
– Risk for Injury
– Self-care Deficit
Kyphosis
• Increase in the curvature of the thoracic
spine outward
• Can develop during the adolescent growth
spurts because of poor posture or
secondary to osteoporosis
• Can impair lung expansion and ventilation
• Treatment: exercises (including back
strengthening), proper posture, bracing,
and surgery
Lordosis
• Exaggerated concave of the lumbar spine
• Can develop during adolescent growth
spurts or because of poor posture
• Obesity can increase risk
• Treatment: exercise, proper posture,
bracing, and surgery
Scoliosis
• Lateral deviation of the spine that may affect the thoracic
or lumbar area or both
• May also include a rotation of the vertebrae
• Stress on the vertebrae causes an imbalance in
osteoclast activity, increasing the curvature during growth
spurts
• May be associated with kyphosis and lordosis
• Varies in severity
• More common in females
• Causes: idiopathic, genetic influences, embryonic
developmental deformities, degenerative diseases,
unequal leg lengths, spinal nerve compression, and
asymmetrical muscle support
Scoliosis
• Complications: pulmonary compromise,
chronic pain, degenerative arthritis of the
spine, intervertebral disk disease, and sciatica
• Manifestations vary depending on the degree
of curvature and are exaggerated when an
affected person bends over
– Include: asymmetrical hip and shoulder alignment,
asymmetrical thoracic cage, asymmetrical gait,
back pain or discomfort, fatigue, and indications of
respiratory compromise
Scoliosis
• Diagnosis: history, physical examination,
spinal X-rays, and a scoliometer
• Treatment: exercises (including back
strengthening), bracing, and surgical
correction (instrumentation or fusion)
Fracture
• A break in the rigid structure of the bone
• Most common traumatic musculoskeletal
disorders
• Causes: falls, motor vehicle accidents,
sports-related injuries and conditions that
weaken the bone (e.g., osteoporosis,
Paget’s disease, and bone cancer)
Types of Fractures
• Simple fracture—a single break with bone
ends maintaining their alignment and
position
– Transverse fracture—straight across the bone
shaft
– Oblique fracture—at an angle to the bone shaft
– Spiral fracture—twists around the bone shaft
Types of Fractures
• Comminuted fracture—multiple fracture
lines and bone pieces
• Greenstick fracture—an incomplete break in
which the bone is bent and only the outer
curve of the bend is broken
– Commonly occurs in children because of
minimal calcification and often heals quickly
• Compression fracture—bone is crushed or
collapses into small pieces
Types of Fractures
• Complete fractures – broken into two or more
separate pieces
• Incomplete fractures - partial break
• Open fractures, or compound fractures – skin
is broken and bone fragments or edges may
be angled and protrude out of the skin
– Cause more soft tissue and increase risk for
infection
• Closed fractures – skin is intact
Types of Fractures
• Impacted fractures – one end of the bone is
forced into the adjacent bone
• Pathologic fractures – result from a weakness
in the bone structure secondary to conditions
such as tumors or osteoporosis
• Stress fractures, or fatigue fractures – occur
from repeated excessive stress
– Common in the tibia, femur, and metatarsals
• Depressed fractures – occur in the skull when
the broken piece is forced inward on the brain
Fracture Healing
1.
2.
3.
4.
Hematoma formation
Necrosis of the broken bone ends
Fibroblasts invade the clot within a few days
Fibroblasts secrete collagen fibers, which form a
mass of cells and fibers called a callus
5. Callus bridges the broken bone ends together
inside and outside over 2–6 weeks
6. Osteoblasts invade the callus and slowly
converts it to bone over 3 weeks to several
months (usually 4–6 weeks)
Complications
• Delayed union, malunion, or nonunion may occur due to poor
nutrition, inadequate blood supply, malalignment, and
premature weight bearing
• Compartment syndrome – a serious condition that results from
pressure increases in a compartment, usually the muscle fascia
in the case of fractures
– Pressure impinges on the nerves and blood vessels contained
within the compartment, potentially compromising the distal
extremity
– Requires prompt identification and treatment to prevent permanent
tissue damage
– Manifestations: excruciating pain that is beyond what would be
expected given the injury
– Diagnosis: measuring pressures inside the muscle fascia
– Treatment: remove the cast (if present) and an immediate
fasciotomy
Complications
• Fat embolism – fat enters the bloodstream, usually after a long
bone fracture
– Can travel to vital organs such as the lungs, brain, or heart, which
can be fatal
– Prevention: early immobilization
• Osteomyelitis – infection of the bone tissue
– Can take months to resolve and result in bone or tissue necrosis.
– Treatment: potent antibiotic therapy (often long-term) and surgery
(e.g., debridement)
• Osteonecrosis, or avascular necrosis – death of bone tissue due
to a loss of blood supply
– Can result from displaced fractures or dislocations
– Treatment: surgical replacement of the necrotic bone and/or joint
Fractures
• Manifestations: deformity (e.g., angulation,
shortening, and rotation), swelling and
tenderness at the site, inability to move the
affected limb, crepitus, pain, paresthesia,
and muscle flaccidity progressing to
spasms
• Diagnosis: history, physical examination,
and X-rays
Fractures
• Treatment: immediate immobilization (e.g.,
splints or traction, reduction (closed or
open), surgery (may include pins, plates,
rods, or screws), debridement, long-term
immobilization (e.g., casts, splints, or
traction), and physical therapy
Dislocations
• Separation of two bones at a joint
• May be complete or partial (subluxation)
• Causes deformity, immobility, and damage to
the nearby ligaments and nerves
• Causes: sudden impact to the joint, congenital
conditions, and pathologic states (e.g., arthritis,
ligament injuries, paralysis, or neuromuscular
disease)
• Most common in the shoulder and clavicle
joints
Dislocations
• Manifestations
– Visibly out-of-place, discolored, or deformed
joint
– Limited movement
– Swelling or bruising
– Intense pain, especially with movement or
weight bearing
– Paresthesia near the injury
• Diagnosis: history, physical examination, Xrays, and magnetic resonance imaging
Dislocations
• Treatment:
– Reduction (spontaneous, gentle manipulation,
or surgery)
– Immobilize the joint with a splint or sling for
several weeks after the reduction
– Analgesics
– Muscle relaxants
– Rehabilitation program (primarily physical
therapy)
– Avoid strenuous activity until full movement,
normal strength, and stability have been
regained
Dislocations
• Immediate treatment:
– Immobilize the area above and below the joint with a splint or sling
in the position the joint was found
– Do not attempt to straighten or move the joint
– Assess for tissue perfusion and report any suspected tissue
perfusion impairment immediately
– Apply ice to ease pain and swelling
– Do not move the person unless the injury has been completely
immobilized
– Do not move a person with an injury to weigh-bearing joints
unless it is absolutely necessary
– Do not give the person anything by mouth
Sprains
• Injury to a ligament that often involves stretching or
tearing of the ligament
• Causes: forcing a joint into an unnatural position
(e.g., twisting one’s ankle)
• Severity described using a grading scale
• Most common in the ankle and knee
• Manifestations: edema, pain, bleeding, joint
stiffness, limited function, disability, and discoloration
(usually bruising)
• Diagnosis: history, physical examination, X-rays, and
magnetic resonance imaging
Sprains
• Treatment:
–
–
–
–
–
–
–
–
Apply ice immediately; wrap the ice in a cloth
Immobilize joint with a splint or an elastic wrap or
Elevate the swollen joint above the level of the heart
Rest the affected joint for several days and gradually
increase activity
Nonsteroidal anti-inflammatory drugs
Keep pressure off the injured area until the pain
subsides (may require crutches when walking)
Repair the ligament tears surgically
Rehabilitate (usually including physical therapy),
beginning within 1 week
Strains
• Injury to a muscle or tendon that often involves
stretching or tearing of the muscle or tendon
• May occur suddenly or develop over time
• Results from an awkward muscle movement or
excess force that can be caused by an accident,
improper use of a muscle, or overuse of a muscle
• Risk factors: excessive physical activity, improper
stretching prior to activity, and poor flexibility
• The lower back is the most common site
Strains
• Severity described using a grading scale
• Manifestations: pain, stiffness, difficulty moving the
affected muscle, skin discoloration (often bruising),
and edema
• Diagnosis: history, physical examination, X-rays,
and magnetic resonance imaging
Strains
• Treatment:
–
–
–
–
–
–
–
–
–
Apply ice immediately; wrap the ice in cloth
Use ice for the first 3 days, and then, either heat or ice
Rest the affected muscle for at least a day
Keep the affected muscle elevated above the level of the
heart (if possible)
Avoid use until pain subsides; then, advance activity
slowly and in moderation
Nonsteroidal anti-inflammatory drugs
Muscle relaxants to relieve muscle stiffness
Surgical repair of severe tendon tears
Rehabilitate
Herniated Intervertebral Disk
• Protrusion of the nucleus pulposus through the
annulus fibrosus
• May occur suddenly or gradually
• Can exert pressure on the spinal cord
• Sensory, motor, or autonomic function may be
impaired depending on the location
• Most frequently involves the lumbosacral region,
but some may involve the cervical disks
• Can result in permanent neurologic damage
Herniated Intervertebral Disk
• Causes: improper body mechanics, lifting
heavy objects, trauma, and degenerative
changes (due to aging and demineralization)
• Manifestations
– May be asymptomatic
– Sciatica
– Pain, paresthesia, or weakness in the lower back
and one leg, or in the neck, shoulder, chest, or arm
– Low back pain or leg pain that worsens by sitting,
coughing, sneezing, laughing, bending, or walking
– Limited mobility
Herniated Intervertebral Disk
• Diagnosis
– Rule out spinal tumors
– Includes: history, physical examination
(including neurologic assessment), spinal Xrays, spinal computerized tomography, spinal
magnetic resonance imaging, nerve conduction
study, myelogram, and electromyography
Herniated Intervertebral Disk
• Immediate treatment: short period of rest,
analgesics, nonsteroidal anti-inflammatory drugs,
muscle relaxants, physical therapy (including
back-strengthening exercises), heat/cold
application, and traction
• Follow-up treatment: injections (e.g., corticosteroid
and chemonucleolysis) into the site, surgical repair
(e.g., diskectomy, laminectomy, and spinal fusion),
and weight loss (if appropriate)
Osteoporosis
• Metabolic condition characterized by a
progressive loss of bone calcium that leaves
the bones brittle
• Can occur due to a decrease in osteoblast
activity or an increase in osteoclast activity
• Spongy bone becomes porous, particularly in
the vertebrae and wrist, and the compact
bone becomes thin
Osteoporosis
• Causes: genetic predisposition, dietary imbalances
(low calcium, protein, vitamin C, and vitamin D intake;
high phosphorus intake), hormonal fluctuations (e.g.,
menopause), and physical inactivity
• Risk factors: advancing age, being female, being
underweight, Caucasian ethnicity, Asian descent,
smoking, excessive alcohol or caffeine consumption,
using certain medications (e.g., corticosteriods,
chemotherapy, thyroid replacements, heparin, and
antacids), certain health conditions (e.g., Cushing’s
disease, thyroid dysfunction, bone tumors,
malabsorption, and anorexia nervosa)
Osteoporosis
• Complications: pathological fractures
(typically in the wrist, hip, and spine)
• Manifestations
– Often asymptomatic in early stages
– Includes: osteopenia, bone pain or tenderness,
fractures with little or no trauma, low back and
neck pain, kyphosis, and height reduction (as
much as 6 inches) over time
Osteoporosis
• Diagnosis
– Conducted screening periodically on those
persons at risk
– Include: history, physical examinations, bone
density scans, X-rays, and spinal computed
tomography
Osteoporosis
• Treatment
– Proper nutrition
– Increasing physical activity (including weight-bearing
activities)
– Eliminating modifiable risk factors
– Pharmacolgy: bisphosphonates, estrogen receptor
modulators, calcitonin, and parathyroid hormone
– Safety measures (e.g., assistive devices, handrails,
removing clutter)
– Pain management
– Surgical repair of fractures or weakened bones
Rickets and Osteomalacia
• Rickets – soft, weak bones in children, usually because of
an extreme and prolonged vitamin D, calcium, or phosphate
deficiency
• Osteomalacia – adult form
• Minerals shift out of the bone if the blood levels become too
low, leading to weak and soft bones
• Risk factors: vitamin D deficiency (e.g., being bedbound,
institutionalized persons, working indoors, strong sunscreen
use, celiac disease, and gastrectomy), dietary imbalances,
genetic influences, renal disease, and liver disease (in
children)
Rickets and Osteomalacia
• Manifestations
– Develop slowly as the bones weaken
– Becomes apparent in children as the soft bones cannot
support the growing child
– Skeletal deformities (e.g., bowed legs, asymmetrical
skull, scoliosis, kyphosis, pelvic deformities, sternum
projection)
– Fractures
– Delayed growth in height or limbs
– Dental problems
– Bone pain
– Muscle cramps or weakness
Rickets and Osteomalacia
• Diagnosis: history, physical examination,
serum mineral levels, serum parathyroid
hormone levels, serum alkaline phosphatase,
X-rays, and bone density study
• Treatment:
– Correcting or managing the underlying cause
– Increase calcium, phosphorus, or vitamin D intake
– Positioning or bracing to reduce or prevent
deformities
– Surgical correction of severe deformities
Paget’s Disease
• Progressive metabolic condition characterized by
excessive bone destruction that occurs along with
the replacement of bone by fibrous tissue and
abnormal bone
• The new bone is bigger but weakened and filled
with new blood vessels
• Results in fragile, misshapen bones
• May occur in one or two areas of the skeleton or
throughout the body
• Often involves long bones, skull, pelvis, and
vertebrae
Paget’s Disease
• The exact cause is unknown, but it is thought
be caused by a virus capable of increasing
osteoclast activity or genetic defects that
produces an increase in interferon-6
• Risk increases with age
• Complications: pathologic fractures,
osteoarthritis, heart failure (related
hypercalcemia and increased cardiac workload
to pump blood to the affected areas),
osteosarcoma, and nerve compression
Paget’s Disease Manifestations
• Vary depending on the
area affected
• Often insidious in onset
and may be
asymptomatic early
• Bone pain
• Skeletal deformities (e.g.,
bowing of the legs,
asymmetrical skull, and
enlarged head)
•
•
•
•
•
•
•
Fractures
Headache
Hearing and vision loss
Joint pain or stiffness
Neck pain
Reduced height
Warmth over the affected
bone
• Paresthesia or radiating pain
in the affected region
• Hypercalcemia
Paget’s Disease
• Diagnosis: history, physical examination, bone
scan, X-rays, serum alkaline phosphatase,
and serum calcium
• Treatment
– Mild cases may only require periodic
monitoring and no treatment
– Pharmacology: bisphosphonates, calcitonin,
nonsteroidal anti-inflammatory drugs, and
analgesics
– Surgery
Osteoarthritis
• Degenerative joint disease characterized by local
deterioration of articulating cartilage and its underlying bone
as well as bony overgrowth
• Cartilage surface becomes rough and worn, interfering with
joint movement
• Tissue damage triggers enzyme release from local cells,
accelerating cartilage disintegration
• Subchondral bone becomes exposed and damaged, and
cysts and osteophytes develop as the bone attempts to
remold itself
• Osteophytes and cartilage pieces break off into the synovial
cavity, further increasing irritation
• Nearby muscles and ligaments may become weakened and
loose
Osteoarthritis
• Results in joint space narrowing, joint instability,
stiffness, and pain
• Most commonly affected are the knees, hips, and
those in the hands and spine
• Not inflammatory in origin, but inflammation
results from the tissue irritation
• Causes: idiopathic and excessive mechanical
stress on the joint (e.g., obesity, overuse, injury,
and congenital musculoskeletal conditions)
• More common in women
Osteoarthritis
• Manifestations
– Gradual onset, usually beginning after the age of 40
– Often develop slowly and worsen over time
– Joint pain that worsens during or after movement or weight
bearing
– Joint tenderness with light pressure
– Joint stiffness, especially upon rising in the morning or after a
period of inactivity
– Enlarged, hard joints
– Joint swelling
– Limited joint range of motion
– Crepitus
– Hard nodules around the affected joint (bone spur
Osteoarthritis
• Diagnosis: history, physical examination, X-rays, and magnetic
resonance imaging
• Treatment
– Goals increase joint strength, maintain joint mobility, reduce
disability, and relieve pain
– Physical therapy
– Weight loss/management
– Ambulatory aids (e.g., walkers and canes)
– Orthopedic devices (e.g., braces and splints)
– Pharmacology: analgesics, nonsteroidal anti-inflammatory drugs,
corticosteroids (either orally or as an intra-articular injection),
glucosamine, chondroitin, and ginger
– Pain management
– Surgery (e.g., arthroscopy, osteotomy, surgical fusion, and
arthroplasty)
Rheumatoid Arthritis
• Systemic, autoimmune condition involving multiple
joints
• Inflammatory process primarily affects the synovial
membrane, but it can also affect other organs
• Often experience remissions and exacerbations,
progressing with each exacerbation
• Usually starts with an acute inflammatory episode
after which the joint may appear to recover
• Pathogenesis: synovitis, pannus formation,
cartilage erosion, fibrosis, and ankylosis
Rheumatoid Arthritis
• The synovium thickens because of the cumulative
effect of the reoccurring inflammation
• The thickened synovium eventually invade and
destroy the cartilage and bone within the joint
• Muscles, tendons, and ligaments weaken and
stretch
• Joints can lose its shape and alignment
• Usually affects joints unilaterally
• Most commonly affects the wrists, fingers, knees,
feet, and ankles
Rheumatoid Arthritis
• The exact cause is unknown, but it is
thought to be caused a genetic
vulnerability that permits a virus or
bacteria to trigger the disease
• Risk factors: being female, family history,
advancing age (however, there is a
juvenile form), and smoking
Rheumatoid Arthritis Manifestations
• Usually insidious onset
Progressively worsen
• Fatigue
• Anorexia
• Low-grade fever
• Lymphadenopathy
• Malaise
• Muscle spasms
• Morning stiffness lasting
more than 1 hour
• Warmth, tenderness, and
stiffness in the joints when not
used
• Bilateral joint pain
• Swollen and boggy- joints
• Limited joint range of motion
• Contractures and joint
deformity (e.g., boutonniere
deformity and swan neck
deformity)
• Unsteady gait
• Depression
• Anemia
Rheumatoid Arthritis
• Diagnosis: history, physical examination,
serum rheumatoid factor test, serum
anticyclic citrullinated peptide antibodies
test, erythrocyte sedimentation rate test,
synovial fluid analysis (rheumatoid factor
is usually present), joint X-rays, joint
magnetic resonance imaging, and joint
ultrasounds
Rheumatoid Arthritis Treatment
• No cure for RA
• Focuses on slowing the progression, managing
the pain, and promoting independence
• Early, aggressive treatment can delay joint
destruction
• Requires a multidisciplinary approach
• Adequate rest and pace activities
• Physical and occupational therapy
• Regular exercise
Rheumatoid Arthritis Treatment
• Pharmacology:
– Nonsteroidal anti-inflammatory drugs
– Corticosteroids (orally or as an intra-articular
injection)
– Disease-modifying antirheumatic drugs (e.g.,
gold compounds, immunosuppressant agents,
and antimalarial agents)
– Biologic response-modifying agents
– Herbal therapies including thunder god vine,
plant oils, and fish oil
Rheumatoid Arthritis Treatment
•
•
•
•
•
•
Nonpharmacologic pain management
Application of heat and cold
Splint and braces
Assistive devices (e.g., walkers and rails )
Coping strategies and support
Surgical repair (e.g., synovectomy and
arthroplasty)
Gout
• Inflammatory disease resulting from deposits
of uric acid crystals in tissues and fluids
• Uric acid is byproduct of breaking down
purines, a substance naturally found in the
body and in certain foods (e.g., organ meats,
shell fish, anchovies, herring, asparagus, and
mushrooms)
• Results from hyperuricemia caused by an
overproduction or underexcretion (most
common) of uric acid
Gout
• Not all people with hyperuricemia have gout
• Most common in males and African Americans
• Causes: inborn error in metabolism, being
overweight or obese, having certain diseases
(e.g., hypertension, diabetes mellitus, renal
disease, and sickle cell anemia), consuming
alcohol (beer and spirits more than wine), using
certain medication (e.g., diuretics), and eating a
diet rich in meat and seafood
Phases of Gout
1. Asymptomatic
–
–
Uric levels climb in the bloodstream and crystals
deposit in the tissue
Crystals accumulate, damaging tissue
2. Acute flares or attack
–
–
–
Tissue damage triggers an acute inflammation
Characterized by pain, burning, redness, swelling,
and warmth at the affected joint lasting days to
weeks
Most initial attacks occur in the lower extremities
(most often the big toe)
Phases of Gout
3. Intercritical period
– After the attack subsides and the disease is clinically
inactive until the next flare
– Hyperuricemia and crystal accumulation continues
– These periods in between attacks become shorter as
the disease progresses
– Reoccurring attacks are often precipitated by sudden
increases in serum uric acid
4. Chronic gouty arthritis
– Characterized by joint soreness and aching present
most of the time
– May also develop tophi that can drain or renal calculi
Gout Manifestations
• Vary depending on the phase
• Intense pain at the affected joint that frequently
starts during the night and is often described as
throbbing, crushing, burning, or excruciating
• Joint warmth, redness, swelling, and tenderness
(even to light touch)
• Fever
• Joint deformities
• Limited joint mobility
Gout
• Diagnosis: history, physical examination,
serum uric acid levels, urine uric acid levels
(will be low in those with gout caused by
underexcretion), synovial fluid analysis
(presence of uric acid crystals), and joint Xrays
Gout Treatment
• Pharmacology for acute gout attacks
– Nonsteroidal anti-inflammatory drugs
– Colchicine
– Corticosteroids
• Pharmacology to prevent the complications
and recurrent episodes
– Xanthine oxidase inhibitors (e.g., allopurinol
[Zyloprim]) to block uric acid production
– Probenecid (Probalan) to improve renal
excretion of uric acid
• Avoiding triggers
Ankylosing Spondylitis
• Progressive inflammatory disorder affecting the sacroiliac
joints, intervertebral spaces, and costovertebral joints
• Inflammation starts in the vertebral joints of the lower back
at the sacroiliac joints and progresses up the spine
• New bone forms in an attempt to remodel the inflammatory
damage
• Results in joint fibrosis and calcification
• Joints become ankylosed
• Vertebrae appear square, and the vertebral column
becomes rigid and losses curvature
Ankylosing Spondylitis
• Genetics seem to be play a role in
development (HLA-B27 gene is present in
most cases)
• More common in males and typically appears
between 20 and 40 years of age
• Complications: kyphosis, osteoporosis,
respiratory compromise, endocarditis, and
uveitis
• May experience periods of remission and
exacerbation
Ankylosing Spondylitis
Manifestations
• Intermittent lower
back pain (early)
• Pain and stiffness that
typically worsens with
inactivity and
improves after activity
• Lower back pain that
evolves to include the
entire back
• Pain in other joints
(especially the
shoulders, hips, or
lower extremities)
• Muscle spasms
• Fatigue
• Low-grade fever
• Weight loss
• Kyphosis
Ankylosing Spondylitis
• Diagnosis: history, physical examination,
serum presence of the HLA-B27 gene,
erythrocyte sedimentation rate test, Xrays, computed tomography, and magnetic
resonance imaging
Ankylosing Spondylitis Treatment
• Goal relieve pain and
stiffness as well as
prevent or delay
complications and spinal
deformity
• Most successful when
initiated before the
disease causes
irreversible damage
• Nonsteroidal antiinflammatory drugs
• Disease-modifying
antirheumatic drugs
• Corticosteroids
• Tumor necrosis factor
blockers
• Muscle relaxants
• Physical therapy
• Surgical repair
• Health promoting lifestyle
behaviors
• Coping strategies and
support
Muscular Dystrophy
• Group of inherited disorders characterized by degeneration
of skeletal muscle
• Nine different forms (including Becker’s MD, Duchenne
MD, myotonic MD, and limb-girdle MD), each with varying
patterns of inheritance and pathogenesis
• Commonality across all types is the presence of a muscle
protein abnormality (dystrophin) that causes muscle
dysfunction, weakness, muscle fiber loss, and
inflammation, and it may involve other tissue (e.g., cardiac
and smooth muscle)
• Fat and fibrosis connective tissue eventually replace
skeletal muscle fibers, progressively weakening the
muscles
Muscular Dystrophy
• Some types are rare, while others are common
• Most types are inherited, but some occur because of a
genetic mutation (often spontaneously)
• Some types cause tremendous disability and rapidly
decline whereas others have minimal symptoms and hardly
noticeable progression
• Some types present in childhood, while others present in
late adulthood
• Duchenne MD is the most common and severe type,
affecting only males (X-linked recessive)
• Complications: cardiomyopathy, recurrent respiratory
infections, respiratory compromise, and death
Muscular Dystrophy Manifestations
• Vary depending on the
type
• All of the muscles may be
affected or only a
selected group
• Mental retardation (in
some types)
• Muscle weakness that
slowly worsens to
hypotonia
• Muscle spasms
• Delayed development of
muscle motor skills
• Difficulty using one or
more muscle groups
•
•
•
•
•
•
•
Poor coordination
Drooling
Ptosis
Frequent falls
Problems walking
Gower’s maneuver
Progressive loss of joint
mobility and contractures
(e.g., clubfoot and foot drop)
• Unilateral calf hypertrophy
• Scoliosis or lordosis
Muscular Dystrophy
• Diagnosis: history, physical examination,
muscle biopsy, electromyelography,
electrocardiogram, serum creatine kinase
levels, serum presence of defective
dystrophin, genetic testing, and fetal
chorionic villus testing (as early as 12 weeks’
gestation)
Muscular Dystrophy
• Treatment
– No cure for MD
– Gene therapy may potentially be the answer
– Goal is to maintain motor function and prevent
deformities as long as possible
– Includes: physical therapy, muscle relaxants,
immunosuppressant agents, assistive devices
(e.g., walker, braces, and splints), surgical
contracture release, coping strategies, and
support
Fibromyalgia
• Syndrome predominately characterized by
widespread muscular pains and fatigue
• Affects muscles, tendons, and surrounding tissue,
but it does not affect the joints
• Eighteen fibromyalgia-specific pressure points,
where pain or tenderness may be stimulated, have
been identified in the neck, shoulder, trunk, and
limbs
• No apparent inflammation or degeneration is
associated with fibromyalgia
Fibromyalgia
• The cause remains uncertain, but may be related
to an altered central neurotransmission that results
in sensitivity to substance P
• The brain’s pain receptors seem to develop a sort
of pain memory and become more sensitive to
pain signals
• Additional causes may be physical or emotional
trauma, sleep disturbances, altered skeletal
muscle metabolism, infections, and genetic
predisposition
• More common in women
Fibromyalgia Manifestations
• May vary depending on the weather, stress,
fatigue, physical activity, and time of day
• Characterized by widespread pain, typically
described as a constant, dull muscle ache
• May also include: fatigue, sleep disturbances,
depression, irritable bowel syndrome, headaches,
and memory problems
• Other conditions that may present include:
rheumatoid arthritis, systemic lupus
erythematosus, and ankylosing spondylitis
Fibromyalgia
• Diagnosis: history (the presence of widespread
pain at least 3 months’ duration and tenderness
on 11 of 18 pressure points), physical
examination, and tests to rule out other conditions
• Treatment: stress reduction, regular exercise,
adequate rest, proper nutrition, heat application,
massage therapy, acupuncture, physical therapy,
analgesics, nonsteroidal anti-inflammatory drugs,
antidepressant agents, antiseizure agents
(specifically pregabalin [Lyrica]), coping
strategies, counseling, and support
Bone Tumors
• The majority are malignant and occur as
secondary tumors from other cancers (e.g.,
breast, lung, and prostate cancers)
• Rarely occur as primary tumors
• The exact cause of primary tumors is
unknown
• Slightly more common in men and
Caucasians
• Risk factors for primary tumors: Paget’s
disease
Bone Tumor Types
• Osteosarcoma
– Aggressive tumor that begins in the bone cells, usually
in the femur, tibia, or fibula
– Occurs most often in children and young adults
• Chondrosarcoma
– Slow-growing tumor that begins in cartilage cells that
are commonly found on the ends of bones
– Most frequently affects older adults
• Ewing’s sarcoma
– Aggressive tumor in which the origin is unknown
– May begin in nerve tissue within the bone
– Occurs most frequently in children and young adults
Bone Tumors
• Manifestations
– Often asymptomatic in early stages
– Include: pathologic fractures, bone pain, and a
palpable mass
• Diagnosis: history, physical examination, X-rays,
computed tomography, magnetic resonance
imaging, positron emission tomography, bone
scan, and biopsy
• Treatment: surgical excision, amputation,
radiation, and chemotherapy