Arthritic Written Report Final

ST.
PAUL UNIVERSITY ILOILO

COLLEGE OF PHYSICAL THERAPY
2014
SEMINAR I
ARTHRITIC CONDITIONS
Leader: Esther Marie Sazon (Adult Rheumatoid Arthritis)

Members: Kimberly Tarucan (Anatomy and Physiology)
Karlyn Denise Casalmir (Juvenile Rheumatoid Arthritis)
Christia Mae Buenaflor (Osteoarthritis)
Samantha Regalado (Seronegative Arthropathies)
Jenny Lou Dormitorio (Crystal Induced Arthropathies)
Mary Noelle Ricablanca (Systemic Lupus Erythematosus)
Tyra Marie Yap Ong (Progressive Systemic Sclerosis)
Jan Paulyn Legaspi (Compilation and Powerpoint)
Reya Kristelle Maalat (Compilation and Powerpoint)
BSPT IV
July 11, 2014
OVERVIEW: ANATOMY AND PHYSIOLOGY
JOINTS
- also called an articulation or arthrosis; is a point of contact between two bones, between bone
and cartilage or between bone and teeth.
Arthrology - scientific study of joints
Kinesiolgy - study of motion of the human body
JOINT CLASSIFICATIONS
Joints are classified structurally; based on their anatomical characteristics, and functionally,
based on the type of movement they permit.
The structural classification of joints is based on two criteria:

1. The presence or absence of a space between the articulating bones, called a synovial
2. The type of connective tissue that binds the bones together.
Fibrous joints : There is no synovial cavity, and the bones are held together by dense
irregular connective tissue that is rich in collagen fibers.
Cartilaginous joints : There is no synovial cavity and the bones are held together by
cartilage.
Synovial joints: The bones forming the joint have a synovial cavity and are united by the
dense irregular connective tissue of an articular capsule, and often by accessory
ligaments.
The functional classification of joints relates to the degree of movement they permit.
Synarthrosis: an immovable joint.
Amphiarthrosis: a slightly movable joint
Diarthrosis: a freely movable joint; all are synovial joints; have variety of shapes and
permit several different types of movements.
STRUCTURE:
1. Fibrous Joints- permit little or no movement
3 Types
Sutures - occur only between bones of the skull.
Syndesmoses - (syndesmo: band or ligament)
- Greater distance between the articulating surfaces and more dense
irregular connective tissue than in a suture
Interosseous Membranes - binds neighboring long bones and permits slight movement
(amphiarthrosis).
2. Cartilaginous Joints- allows little or no movement; articulating bones are tightly connected by
either hyaline cartilaginous or fibrocartilage.
2 Types
Synchondrosis - (chondro: cartilage)
- cartilaginous joint in which the connecting material is hyaline cartilage.
-immovable (synarthrosis)
Symphysis- (growing together)
- ends of the articulating bones are covered with hyaline cartilage but
a broad, flat disc of fibrocartilage connects the bones.
- slightly movable joint (amphiarthrosis)
3. Synovial Joints - there is a presence of a space called a synovial (joint) cavity between the
articulating bones.
- free movable (diarthrosis)
- bones at a synovial joint are covered by a layer of hyaline
cartilage called articular cartilage.
6 Types
Plane joints - a.k.a planar joint, are flat or slightly curved.
- primarily permit back-and-forth and side-to-side movements
between the flat surfaces of bones, but may also rotate against one
another.
o Biaxial - permit movement in two axes.
o Triaxial (multiaxial) - plane joints rotate in addition to sliding; permit movement in three
axes.
Hinge joints - a.k.a ginglymus joint; the convex surface of one bone fits into the concave
surface of another bone.
- Uniaxial (monoaxial) typically allow motion around a single axis.
Pivot joints - a.k.a trochoid joint; the rounded or pointed surface of one bone articulates
with a ring formed partly by another bone and partly by a ligament.
- Uniaxial, because it allows rotation only around its own longitudinal axis.
Condyloid joints - (condyl=knuckle) or ellipsoidal joint, the convex oval-shaped
projection of one bone fits into the oval-shaped depression of another bone.
- Biaxial (flexion-extension, abduction-adduction) + limited
circumduction.
Saddle joints - a.k.a sellar joints; articular surface of one bone is saddle-shaped, and the
articular surface of the other bone fits into the saddle.
- Biaxial(flexion-extension, abduction-adduction) + limited
circumduction
Ball-and-Socket Joints - a.k.a spheroid joint consists of the ball-like surface of one bone
fitting into a cuplike depression of another bone.
- Triaxial (multiaxial) (flexion-extension, abduction-adduction,
and rotation)
I.-II. DEFINITION OF TERMS
Arthritis - inflammation of the joints
Rheumatoid arthritis or RA - a systemic rheumatic disease characterized by an acute
inflammatory response; a major sub classification within the category of diffuse
connective tissue disease; the pathologic process of RA has impact on joints, their
surrounding structures, and other major organ systems.
INCIDENCE
One of every 50 adults in the population
It has been estimated that the prevalence rate of definite RA among adults in the
United States is approximately 10 cases per 1000 people, or approximately 2.1
million persons.
Affects women of two to four times more often than men at all ages.
General increase in the prevalence for both sexes with increasing age.
CLASSIFICATION
Adult Rheumatoid
Juvenile Rheumatiod Arthritis
III. ETIOLOGY
The cause of Rheumatoid Arthritis is still unknown.
Scientists have developed a number of theories which are the following:
1. The first theory suggests that the body inadvertently alters its defense mechanisms
so as to attack its own joint linings - the synovial membranes. This explanation
comes from the observation that the joint linings show changes that are similar to
those seen in any part of the body in which an antibody reaction is involved in
resisting a virus. This resistance is due to the development of antibodies against
the particular infection. Immunity, therefore, has a very important task in the
body. But it can be very harmful, or even destructive, in other circumstances. In
rheumatoid arthritis, for some particular reason, the bodys defense mechanism
may react against the joint lining in a similar way. The joint lining becomes
inflamed and damages the joint.
2. The second theory is that RA is directly caused by some type of persistent
infection. There are a number of known infections in animals in which the
invading organisms enter joints to produce inflammation that is similar in some
respects to rheumatoid arthritis.
3. The third theory combines the other two. An infection damages the joint so much
that the body no longer recognizes it as its own tissues. So it develops antibodies
against the damaged joint.
PATHOMECHANISM
Immune complexes produced by synovial lining cells and in inflamed blood vessels.
Plasma cells produce antibodies (eg, rheumatoid factor [RF], anticyclic citrullinated
peptide antibody [anti-CCP]) that contribute to these complexes, but destructive
arthritis can occur in their absence.
Macrophages also migrate to diseased synovium in early disease; increased
macrophage-derived lining cells are prominent along with vessel inflammation.
Lymphocytes that infiltrate the synovial tissue are primarily CD4+ T cells.
Macrophages and lymphocytes produce pro-inflammatory cytokines and chemokines
(eg, tumor necrosis factors [TNF], granulocyte-macrophage colony-stimulating
factor [GM-CSF], various ILs, interferon-) in the synovium.
In chronically affected joints, the normally thin synovium proliferates, thickens, and
develops many villous folds. The synovial lining cells produce various materials,
including collagenase and stromelysin, which contribute to cartilage destruction, and
IL-1 and TNF-, which stimulate cartilage destruction, osteoclast-mediated bone
absorption, synovial inflammation, and prostaglandins (which potentiate
inflammation).
Hyperplastic synovial tissue (pannus) releases these inflammatory mediators, which
erode cartilage, subchondral bone, articular capsule, and ligaments. PMNs on
average make up about 60% of WBCs in the synovial fluid.
Rheumatoid nodules develop in about 30% of patients with RA. They are
granulomas consisting of a central necrotic area surrounded by palisaded histiocytic
macrophages, all enveloped by lymphocytes, plasma cells, and fibroblasts. Nodules
and vasculitis can also develop in visceral organs.
IV. SIGNS AND SYMPTOMS

Morning stiffness lasting for more than 3 minutes (hallmark)
Muscle atrophy
Anorexia, weight loss, and fatigue
Bilateral and symmetrical pattern of joint involvement
Immobility and the cardinal signs of inflammation.
Joint pain or Arthralgia
Crepitus, which is the audible or palpable grating or crunching as the joint is
moved through its range of motion.
Restricted movement, painful and deformity in specific joints of the body such
as finger joints, wrist joints, knee joints, those at the bases of the toes, and the
joints in the body that contain this particular tissue lining called synovial
membrane.
- Wrists and the index (2nd) and middle (3rd) metacarpophalangeal
joints (most commonly involved)
- Proximal interphalangeal joints
- Metatarsophalangeal joints
- Shoulders
- Elbows
- Hips
- Knees
- Ankles
Development of small lumps called nodules which can grow and become
tender.
Tenosynovitis that interferes with the smooth gliding of tendon on the tendon
sheath
DIFFERENTIAL DIAGNOSIS
Many disorders can simulate RA:
RF can be nonspecific and is often present in several autoimmune diseases;
the presence of anti-CCP antibodies is more specific for RA. For example,
hepatitis C can be associated with an arthritis similar to RA clinically and that
is RF-positive; however, anti-CCP is negative.
Some patients with crystal-induced arthritis may meet criteria for RA;
however, synovial fluid examination should clarify the diagnosis. The
presence of crystals makes RA unlikely. Joint involvement and subcutaneous
nodules can result from gout, cholesterol, and amyloidosis as well as RA;
aspiration or biopsy of the nodules may occasionally be needed.
SLE usually can be distinguished if there are skin lesions on light-exposed
areas, hair loss, oral and nasal mucosal lesions, absence of joint erosions in
even long-standing arthritis, joint fluid that often has < 2000 WBCs/L
(predominantly mononuclear cells), antibodies to double-stranded DNA, renal
disease, and low serum complement levels. In contrast to RA, deformities in
SLE are usually reducible because of the lack of erosions and bone or
cartilage damage. Arthritis similar to RA can also occur in other rheumatic
disorders (eg, polyarteritis, systemic sclerosis, dermatomyositis, or
polymyositis) or there can be features of more than one disease, which
suggests an overlap syndrome or mixed connective tissue disease.
Sarcoidosis, Whipple disease, multicentric reticulohistiocytosis, and other
systemic diseases may involve joints; other clinical features and tissue biopsy
sometimes help differentiate these conditions. Acute rheumatic fever has a
migratory pattern of joint involvement and evidence of antecedent
streptococcal infection (culture or changing antistreptolysin O titer); in
contrast, RA has an additive arthritis.
Reactive arthritis (see Reactive Arthritis) can be differentiated by antecedent
GI or GU symptoms; asymmetric involvement and pain at the Achilles
insertion of the heel, sacroiliac joints, and large joints of the leg;
conjunctivitis; iritis; painless buccal ulcers; balanitis circinata; or keratoderma
blennorrhagicum on the soles and elsewhere.
Psoriatic arthritis (see Psoriatic Arthritis) tends to be asymmetric and is not
usually associated with RF, but differentiation may be difficult in the absence
of nail or skin lesions. DIP joint involvement and severely mutilating arthritis
(arthritis mutilans) is strongly suggestive, as is the presence of a diffusely
swollen (sausage) digit. Ankylosing spondylitis (see Anklyosing Spondylitis)
may be differentiated by spinal and axial joint involvement, absence of
subcutaneous nodules, and a negative RF test.
Osteoarthritis (see Osteoarthritis (OA)) can be differentiated by the joints
involved; the absence of rheumatoid nodules, systemic manifestations, or
significant amounts of RF; and synovial fluid WBC counts < 2000/L.
Osteoarthritis of the hands most typically involves the DIP joints, bases of the
thumbs, and proximal interphalangeal joints. RA does not affect the DIP
joints.
V. ANCILLARY PROCEDURES
Two concepts:
1. Sensitivity test - done to avoid a false negative result
2. Concept of specificity - a laboratory test that measures the ability to avoid false
positives.
1. Elevated erythrocyte sedimentation rate (ESR) or C reactive protein (CRP), acute
phase reactants, indicates the presence of active inflammation. Although it is
characteristic that patients with RA have an active inflammation, up to 40 percent
of the patients with RA have normal values for these tests despite marked clinical
evidence of inflammation. Normal ESR and CRP values do not exclude a
diagnosis, nor do elevated levels signify a diagnosis of RA. Rheumatoid factor
(RF) is the result of the binding of two immunoglobulins. The presence or
absence of RF neither confirms nor rules out the diagnosis of RA. A positive RF
cannot confirm a RA; however in combination with the clinical criteria, positive
RF can confirm a clinical impression.
2. A complete blood count (CBC) is routinely ordered because of the findings are
commonly associated with RA. Red blood cell counts are often decreased,
indicating the anemia of chronic disease found in approximately 20 percent with
RA. By comparison, the white blood cell count is generally normal.
Thrombocytosis, a high platelet count, is not uncommon for RA.
3. A synovial fluid analysis can greatly enhance the process of differential diagnosis.
A culture can be done to identify the potential bacterial agents as a cause of joint
inflammation. Inflammatory arthritis, such as RA, produces fair mucin clotting.
4. Radiographic study is an essential component of the diagnostic workup for RA.
Radiographic changes may indicate the presence of RA in a certain joint when
there is an uneven, reduced, or loss of cartilage or erosion of some joint surfaces.
Diagnostic confirmation is available only later in the disease process when the
typical joint space narrowing and erosions in the hands and feet are seen in the
characteristic bilateral distribution.
PT EVALUATION
The PT should begin an examination by taking a patient history that will orient the
therapist to the nature and extent of the current problem and relate that problem to
the patients past medical history.
During the interview, the PT must elicit to the patient the individuals understanding
of the disease and what is personally seen as the major problem at hand.
The therapist must also take note of the signs and symptoms of the patient and pain
should be examined in terms of its location, duration and intensity. Joint symptoms,
morning stiffness, previous level of activity and current medication regimen should
also be noted.
Following the history, a review of the cardiopulmonary, integumentary, and
neuromuscular systems should be undertaken before performing definitive
examination of the musculoskeletal system which are the following:
Range of motion
Strength
Joint stability
Endurance
Functional examination
Gait and mobility
Sensory integrity
Psychological status
Environmental barriers
VI. TREATMENT
Medical
In RA, joint destruction and irreversible damage are most pronounced in the first years
after the disease onset.
Nonsteroidal anti-inflammatory drugs (NSAIDs)
- Basic element in long term treatment of RA; analgesic (lower dose
effect) and anti-inflammatory actions (higher dose effect)
- Does not alter the underlying disease process
Disease-modifying antirheumatic drugs (DMARDs)
- heterogeneous group of drugs exhibiting a wide range of chemical
structure, modes of actions, clinical indications, and toxicities
- Biologics or biologic response modifying (BRM) agents (new group),
have proved to be effective and offer the possibility of controlling
rheumatic diseases to an extent not previously possible; blocks either
tumor necrosis factor alpha or interleukin 1
Corticosteroids
- analogues of the naturally occurring hormone cortisone and are most
powerful anti-inflammatory drugs available; can be given systematically or
periarticular injection
- limited to no more than two to four per year to reduce the risk of
osteonecrosis and soft tissue damage.
Surgical treatment for RA
Synovectomy - early stages of arthritis, the inflamed synovium or joint
lining may be removed
PT
Maintain and improve the range of the movements of the joints and to increase the
strength of the muscles that control them.
Modalities for pain relief to manage pain and facilitate more comfortable
exercise and physical activity.
Superficial heat is used to produce localized analgesia and increase local
circulation in the area to which it is applied. This can be delivered through:
moist hot packs, dry heating pads and lamps, paraffin, and hydrotherapy.
Paraffin is particularly useful in delivering superficial heat to irregularly
shaped joints or to the individuals who cannot tolerate the weight of the moist
hot pack. Hydrotherapy is one way of coping with then problem of weight. It
may orient the patient to the value of therapeutic aquatic program that can be
undertaken in conjunction with or following treatment.
Local application of cold will also produce local analgesia and increase in
superficial circulation at the site of application following an initial period of
vasoconstriction. Therapists may either use wet or dry applications.
Patients must be encouraged to perform self-ROM to the extent possible to
maintain motion. Therapists may apply neurophysiological principles of
therapeutic exercise to lengthen shortened muscles. Patients should also be
given the opportunity to rest frequently while performing the exercise.
Therapists are also to let the patient perform isometric exercise and dynamic
exercise to improve the strength and function.
Therapists should also target functional activities that require specific
techniques of joint protection. In addition to reducing pain and improving
function, orthoses also may provide support and protection for vulnerable and
painful joints.
Endurance and functional training should also be part of the therapeutic
program in order for the patients to increase their self-esteem and physical
activity levels, and as well as for them to be able to perform their activities of
daily living effectively.
JUVENILE RHEUMATOID ARTHRITIS
I-II. DEFINITION OF TERMS:

JUVENILE RHEUMATOID ARTHRITIS
- a.k.a Juvenile Idiopathic Arthritis
- Affecting children younger than age 16
- an inflammatory disorder of the connective tissues, characterized by joint
swelling and pain or tenderness
- Characterized by synovitis of the peripheral joints, soft tissue swelling, and
effusion
- Can influence epiphyseal growth, resulting in discrepancy in leg length
- Generalized stunted growth may occur
- It may also involve organs such as the skin, heart, lungs, liver, spleen, and eyes,
producing extra-articular signs and symptoms
- Joint stiffness in the morning or after periods of inactivity (common)
Has three major types:
Systemic
Polyarticular
Pauciarticular
INCIDENCE
- Considered as the major chronic rheumatic disorder of childhood
- May occur as early as age 6 weeks but seldom before age 6 mos; peak onset
between ages 1 and 3 and 8 and 12
- Affects an estimated 1,500,000 to 250,000 children in the US
- Overall incidence is twice as high in female with variation among the types of
JRA
CLASSIFICATION
SYSTEMIC
- Often called as Stills disease
- Almost all children with this type of JRA test negative for both RF and ANA.
- Also affect internal organs such as the heart, liver, spleen and lymph nodes.
- Child may experience mild, transient arthritis or frank poly-arthritis associated with
fever and rash
- Symptoms usually subside in 6 to 12 mos
- Joint involvement may not be evident at first, but the childs behavior may clearly
suggest joint pain and fatigue
- Can also make an initial appearance in adulthood
POLYARTICULAR
- About 30% of all children are affected with this type
- Affects five or more joints during the the first 6 mos. of the disease
- The small joints, such as those in the hands and feet, are most commonly involved,
but the disease may also affect large joints
- Polyarticular JRA often is symmetrical; that is, it affects the same joint on both
sides of the body
- Some children with polyarticular disease have a special kind of antibody in their
blood called IgM rheumatoid factor (RF)
PAUCIARTICULAR
- 4 or fewer joints are affected
- Most common form of JRA; about half of all children with JRA have this type
- Typically affects large joints, such as the knees
- Girls under age 8 are most likely to develop this type of JRA
- Some children have special proteins in the blood called Antinuclear antibodies
(ANAs)
- Many children with pauciarticular disease outgrow arthritis by adulthood, although
eye problems can continue and joint symptoms may recur in some people.
Affects two distinct groups:
1. Consist of girls younger than 6 years of age with chronic uveitis. The result of
Anti-Nuclear Antibodies (ANA) testing in this group is usually positive.
2. Characterized by late-onset arthritis, is made up of mostly boys. Human
Leukocyte Antigen (HLA-B27) test results are positive. They are affected by
sacroiliitis, and the arthritis usually occurs in the lower extremities.
III. ETIOLOGY
Unknown
Possible genetic factors or an abnormal immune response
Viral or bacterial (particularly streptococcal) infection
Trauma
Emotional stress
PATHOMECHANISM
If JRA is not arrested, the inflammatory process in the joints occurs in four stages:
1. Synovitis develops from congestion and edema of the synovial membrane and joint
capsule.
2. Pannus covers and invades cartilage and eventually destroys the joint capsule and
bone.
3. Fibrous tissue and ankylosis occludes the joint space.
4. Fibrous tissue calcifies, resulting in the bony ankylosis and total immobility

SYSTEMIC JRA
Behavioral clearly suggestive of joint pain (child may want to constantly sit in a
flexed position, may not walk much, or may refuse to walk at all)
Evanescent rheumatoid rash: small, pale or salmon pink macules most commonly in
the trunk and proximal extremities an occasionally on the face, palms, and soles
(with fever); intensifies with massage or application of heat
Fever (sudden onset, spiking to 103F [39.4] or higher once or twice per day-
usually in the late afternoon-rapidly returning to Normal or subnormal)
Hepatosplenomegaly
Irritability
Listlessness
Lymphadenopathy
Myocarditis
Nonspecific abdominal pain
Pericarditis
Pleuritis
POLYARTICULAR JRA
Developmental retardation
Hepatosplenomegaly
Listlessness
Low-grade fever with daily peaks
Lymphadenopathy
Subcutaneous nodules on the elbows
Swollen, stiff, tender joints (most commonly in the wrists, elbows, knees, ankles,
small joints of the hands and feet and, possibly, the temperomandibular joints and
those of the cervical spine, hips, and shoulders)
Weight loss
PAUCIARTICULAR
CHRONIC IRIDOCYCLITIS
Typically asymptomatic inflammation of the iris and ciliary body (but possible pain,
redness, blurred vision, and photophobia.
SACROILIITIS
Lower-extremities; hip, sacroiliac, heel, and foot pain
Achilles tendinitis
Sacroiliac and lumbar arthritis
Acute iritis
JOINT INVOLVEMENT BUT NEGATIVE FOR ANAs and HLA-B27 and WITHOUT
IRITIS
Asymmetrical involvement of large or small joints
Progression to polyarticular disease is possible.
Leukemia is the single most important disease that is mistaken for juvenile idiopathic
arthritis (JIA)
Patients with acute lymphocytic leukemia can present with joint pain and arthritis
Expansion of lymphoblasts in bone metaphyses results in pain, which is typically severe and
may awaken the child from sleep Septic Arthritis affects usually one joint; fever,
systematically unwell and inability to bear weight are common features
Systemic Lupus Erythmatosus (SLE) - characterized by joint and muscle pain, often
with early morning stiffness
Juvenile Dermatomyositis a systemic, autoimmune inflammatory muscle disorder
and vasculopathy that affects children younger than 18 years; characterized by skin
rash and muscle weakness.
Laboratory tests are useful for ruling out other inflammatory or even malignant disease
that can mimic JRA and for monitoring disease activity and response to therapy.
Complete Blood Count shows decreased hemoglobin levels, neutrophilia, and
thrombocytosis.
Erythrocyte Sedimentation Rate, complement(C)- reactive protein, haptoglobin,
immunoglobulin, and C3 levels may be elevated.
Test results may be positive for ANAs patients who have pauciarticular JRA with
chronic iridocyclitis
RF is present in 15% of patients with JRA, as compared with 85% of patients with
RA
Positive HLA-B27 test result mat forecast later development of ankylosing
spondylitis.
Early X-ray changes include soft-tissue swelling, effusion, and periostitis in
affected joints. Later, osteoporosis and accelerated bone growth may appear,
followed by subchondral erosions, joint space narrowing, bone destruction, and
fusion
PT Evaluation
Promotes regular exercise to maintain joint mobility and muscle strength , thereby
preventing contractures, deformity, and disability. Good posture, gait training, and joint
protection are beneficial.
VI. TREATMENT
Medical
Successful management of JRA usually involves administration of anti-
inflammatory, physical therapy, carefully planned nutrition and exercise, and
regular eye examinations.
Non-Steroidal Inflammatory Drugs (NSAIDs)- such as Aspirin, Ibuprofen, or
Naproxen (Aleve)- is used to reduce pain and swelling.
Disease-Modifying Antirheumatic Disease (DMARDs) such as Methotrexate
(Trexall) is useful in second-line agent. In addition, Gold salts,
Hydroxychloroquine (Plaquelin), Auronofin (Ridaura), Etenercept (Enbrel), or
Sulfasalazine (Azulfidine) may be considered. Responses among the given drug
may differ among the various types of JRA.
(For adverse effects) Systemic steroids are usually reserved for treatment of
systemic complications that are resistant to NSAIDs and DMARD, such as
pericarditis and iritis. However, an intra-articular steroid can be effective in
managing pauciarticular and polyarticular JRA.
Corticosteroids and Mydriatics are commonly used for iridocyclitis. Low-dose
cytotoxic drug therapy is currently being investigated.
Surgery is usually limited to soft-tissue releases to improve joint mobility, joint
replacement is delayed until the child has matured physically and can handle
vigorous rehabilitation.
PT
Joint rest (by splinting) used for to 3 days after joint injections with a corticosteroid
may improve anti-inflammatory response.
Splints help reduce pain, prevent contractures, and maintain correct joint alignment
OSTEOARTHRITIS
I-II. DEFINITION OF TERMS

DEGENERATIVE JOINT DISEASE
Osteoarthritis - form of chronic arthritis found commonly in middle aged and elderly
people, affecting especially the weight bearing joints and characterized by
degenerative changes in articular cartilages and bony overgrowth at the joint
margins.
Primary Osteoarthritis - used to designate cases in which no underlying cause for the
joint disease is clearly apparent.
Secondary Osteoarthritis - an antecedent disease or injury is believed to be related to
the arthritis may result from any condition that disturbs normal joint function,
including burnt out RA, repeated trauma, malalignment as a result of fractures, and
congenital subluxation of the hip; frequently seen in a younger age range than in the
primary disease.
INCIDENCE
The age standardized prevalence of radiographic knee OA in adults age 45 was
19.2% among the participants in the Framingham Study and 27.8% in the Johnston
County Osteoarthritis Project. In the third National Health and Nutrition Examination
Survey (NHANES III), approximately 37% of participants age >60 years or older
had radiographic knee OA.
Age-standardized prevalence of radiographic hand OA was 27.2% among the
Framingham participants
Radiographic hip OA was less common than hand or knee OA.
III. ETIOLOGY
Includes mechanical, dystrophic, and genetic factors.
Degenerative changes in articular cartilage are more common and more severe with
advancing age, in the weight-bearing joints and in joints that have become
incongruent or have been used abnormally.
The role of repetitive microtrauma in etiology of OA has also received attention.
Obesity has been shown to be a risk factor for the development of OA in later life.
PATHOMECHANISM
Appears in articular cartilages rather than in the synovial membrane; the cartilage
seems to lose some of its ability to withstand mechanical stresses.
The cartilage undergoes splitting, fibrillation, gradual thinning, and widespread
degeneration. Loss of metachromatic staining in the superficial layers of cartilage
suggests a depletion of proteoglycan matrix.
In early stages, there is an increased production of protein polysaccharide by
proliferating cartilage cells in the deeper layers, perhaps as a compensation for the
matrix loss. The protein polysaccharide ride of youthful cartilage is almost entirely
chondroitin-4-sulfate.
As cartilage ages, there are increasing amount of keratin sulfate and chondroitin-6-
sulfate in the matrix which may alter its mechanical properties. The large
proteoglycan-hyaluronate aggregates account for many of the excellent mechanical
properties of normal articular cartilage.
In OA, diminished binding of proteoglycan to hyaluronic acid cores results in shorter
chains, which in turn reduces the compressive stiffness and resiliency of the
cartilage.
In late stages, the underlying bone may be denuded. About the joint margins, reactive
chondro-osseous spicules or osteophytes form quite early, these appear in
roentgengrams as spurs and lipping.
Occasionally, there is a mild inflammatory reaction, possibly caused by particles of
joint debris engulfed by the synovial tissue. The amount of synovial fluid may
remain normal but may increase considerably if the joint is subjected to excessive
use or minor injury, thus the synovial membrane and periarticular tissues often show
little change but may become considerably thickened.

Early Stage
Stiffness with aching pain
Slight enlargement of affected joints in the fingers and knees; Heberdens nodes (DIP
enlargement, one of the most common signs); Bouchards Nodes (PIP enlargement)
Late Stage
Limitation of joint motion
Pain may be present while the joint is at rest
Malalignment of the joint
Crepitation may be noticed frequently most especially in the knee that may produce
transient locking.
Examination reveals moderate swelling and puffiness with loss of the normal joint
occur.
Early Fatigue
DIAGNOSIS
Made after careful analysis of history and of the joint changes shown by physical and
roentgengraphic examination.
Imaging studies
Plain radiography - The imaging method of choices; cost-effective and can be
readily and quickly obtained; In the load-bearing areas, radiographs can depict
joint-space loss, as well as subchondral bony sclerosis and cyst formation
Computed tomography (CT) scanning - Rarely used in the diagnosis of primary
osteoarthritis; it may be used in the diagnosis of malalignment of the
patellofemoral joint or of the foot and ankle joints
Magnetic resonance imaging (MRI) - Not necessary in most patients with
osteoarthritis unless additional pathology amenable to surgical repair is suspected;
can directly visualize articular cartilage and other joint tissues (e.g., meniscus,
tendon, muscle, or effusion)
Ultrasonography - Being investigated as a tool for monitoring cartilage
degeneration; can be used for guided injections of joints not easily accessed
without imaging
Bone scanning - Helpful in the early diagnosis of osteoarthritis of the hand; can
also help differentiate osteoarthritis from osteomyelitis and bone metastases
PT Evaluation
PT should carefully review the chart, begin an examination by taking the patient
history that will orient the therapist to the nature and extent of the current problem
and relate that problem to the patients past medical history
PT should elicit from the patient that individuals understanding of the disease and
what is personally seen as major problem.
PT should be concerned in identifying the signs and symptoms that indicate the need
for immediate medical follow up. Pain should be examined also in terms of location,
duration and intensity along with the other signs of inflammation. Specific
information on joint symptoms, morning stiffness, previous level of activity, pattern
and degree of fatigue and current medication regimen should also be gathered.
Lastly, following the history, a review of the cardiopulmonary, integumentary, and
neuromuscular systems should be undertaken before performing more definitive
examination of the musculoskeletal system.
PT should also examined the patients:
- Range of Motion
- Strength
- Joint Stability
- Endurance
- Functional Examination
- Mobility and Gait
- Sensory Integrity
- Psychological Status
- Environmental Barriers
There is no specific laboratory test to diagnose OA. It is diagnosed using someone's
personal and family medical histories, a physical exam, X-rays, and in some cases with
an examination of synovial fluid from an affected joint.
Tests that may be ordered to rule out other conditions and to evaluate the person's health
include:
1. Rheumatoid factor (RF) and Cyclic citrullinated peptide antibody (CCP) to help
diagnose rheumatoid arthritis (RA) and differentiate it from osteoarthritis; both
tests are positive with RA and generally negative in OA.
2. Synovial fluid analysis to look for signs of joint infection and to detect
monosodium urate (uric acid) crystals that could indicate gout or calcium
pyrophosphate crystals that may contribute to joint damage in osteoarthritis.
3. Erythrocyte sedimentation rate (sed rate or ESR) to detect inflammation in the
body; ESR will be increased in RA but not in osteoarthritis.
4. C-reactive protein (CRP) to detect inflammation and test for the activity of the
disease; may be used to help differentiate osteoarthritis and RA; an increased
level of CRP occurs in RA but not in osteoarthritis.
5. Complete blood count (CBC) to help evaluate red and white blood cells and
hemoglobin; may be ordered to monitor the side effects of some OA treatments
6. Comprehensive metabolic panel (CMP) to help evaluate and monitor kidney
and liver function
VI. TREATMENT
Medical
1. General measures The patient must be also taught to adjust physical activity to a
level that the affected joints will tolerate; should be instructed in a simple program of
brief range-of-motion, non-weight bearing exercises done once or twice daily, will do
much to maintain joint mobility, ameliorate or to make something better the symptoms
and improve body mechanics. Gradual reduction of weight by dieting is frequently
indicated.
2. Drug therapy Aspirin is the drug of choice and may be given of one to three 325-mg
tablets 3 to 5 times daily. Phenylbutazone may be use but because of its potential toxicity
must be carefully controlled. Since OA, is essentially a non-inflammatory disorder, these
drugs are used for analgesic effects.
3. Local treatment of joints For weight bearing joints, either a restriction of standing
and walking or the temporary use of crutches or cane may be indicated. Local rest may be
facilitated by means of a splint or brace but no joint should be completely fixed for long
periods. Brief periods of mild traction are frequently helpful in relieving symptoms,
particularly in arthritis of the cervical spine and the hip.
4. Prevention of deformity Most of the deformity is caused by changes in shape of the
articular ends of the bones. At times, however, the hips may become flexed and adducted,
the kness may developed flexion, varus or valgus deformity and the feet may become
pronated. Selected exercises and splinting can help prevent such deformities.
5. Surgical measures In OA, surgical treatment is often indicated if the joint changes
have become so advanced that non-operative measures no longer control the symptoms
effectively. Operations are used primarily to relieve pain on motion and secondarily to
correct deformity, restore mobility or provide stability. Osteotomy is often helpful in
improving alignment and relieving pain or removing loose bodies which occasionally
appear in osteoarthritic joints that causes pain and locking. Arthrodesis or the fusion of a
joint between two or more bones on the other hand is useful in monoarticular secondary
arthritis and the Arthroplasty or the surgical repair of a joint may relieve pain without
producing stiffness.
PT
1. Modalities for Pain Relief
- The primary purpose of these modalities is to manage pain and facilitate more
comfortable exercise and physical activity. Superficial heat is used to produce localized
analgesia and increase local circulation in the area to which it is applied and can be
delivered through a number of means such as moist hot pack, dry heating pads and
lamps , paraffin and hydrotherapy but it penetrates only a few millimeters and does not
enter the depth of synovial cavity. In the other hand, local applications of cold will also
produce local analgesia and increase superficial circulation at the site of application
following an initial period of vasoconstriction. Cold is particularly useful around joints
that are swollen, a condition that is usually worsens with the application of superficial
heat modalities. Orthoses may also be used to alleviate pain through biomechanical
support or correction for individuals with knee OA. Foot orthoses designed to reduce
calcaneal valgus or foot pronation and reduce mechanical stress on the knee.
2. Joint Mobility
- Patients should be taught of proper positioning when resting and should be encouraged
to perform self-ROM to the extent possible to maintain motion. Patients should be also
given the opportunity to rest frequently when performing the exercises and pain should
be respected at all times and should be minimal after exercises but if the patient
complains discomfort in excess of 1 hour, it is a potential indicator that either the
intensity or duration of the exercise was too great and should be reduce on the next
session.
3. Strengthening
- In persons with knee OA, the evidence is strong and consistent that LE exercise that
includes neuromuscular and functional training reduces pain and improves function.
Interventions have included isometric, isotonic and functional exercises, as well as
proprioceptive and balance training and have been tested in both clinically supervised and
self-directed settings with positive results and acceptable adherence.
4. Endurance Training
- If weight bearing is a barrier to exercise, a non-weight bearing apparatus such as cycle
ergometry or aquatic program may be used. For most people, walking and stationary
bicycles are safe and effective means of aerobic exercises.
5. Functional Training
- PT may choose to reduce the functional demands of an activity either temporarily such
as under conditions of acute inflammation or permanently by incorporating a variety of
aids into ADL that substitute loss ROM and strength. These modifications can include
long-handled appliances and devices with build-up handles for easier grasp. There are
aids for dressing and grooming as well as personal hygiene that can help increase
individuals independence.
6. Gait training
- May include gait asymmetries, decreased velocity, cadence, and stride length, prolonged
period of double support, inadequate heel strike and toe off and diminished joint
excursion through both swing and stance because through this a PT can able to know
what he / she will do for the good of the patient or how he / she will give the treatment
specifically for patients with OA.
7. Education
Patient education in the rheumatic diseases has been shown to result positive changes in
knowledge, health behaviors, beliefs and attitudes that affects health status, quality of life
and health care utilization.
CLASSFICATIONS OF OSTEOARTHRITIS
1. Osteoarthritis of the Spine
INCIDENCE AND ETIOLOGY
Extremely common
Seen most often in stocky and obese persons over 40 years of age
More frequent in males than females and much more common than either RA of the
spine or ankylosing spondylitis
Often observed in the lumbar and cervical levels of the spine
The repeated minor traumas of constant use of the back are probably an important
causative factor; faulty body mechanics probably play a part by putting added strain
on localized areas of the spine
Degenerative disk disease, ruptured nucleus pulposus and OA in the spine may be
related manifestations of similar disease process.
PATHOMECHANISM
Takes place in the spinal diarthrodial and in the intervertebral joints
Eburnation of bone and spur formation may occur about the articular facets, thinning
of the intervertebral disks and spur formation at the antero-lateral margins of the
vertebral bodies result from disk degeneration and reactive bone production; often
term as spondylosis usually accompany OA of the facet joints.
In later stages, the vertebral bodies become flattened and much new bone develops
about their margins, producing so-called bridging and leaf formation.
SIGNS AND SYMPTOMS
Stiffness and pain in the neck and lower back.
Numbness and weakness of the arms or legs
DIAGNOSIS
From the history, the physical findings, and the associated roentgenographics
changes of lippins, spurs and irregular bone formation about the vertebral margins
Must also be differentiated from neurogenic arthropathy and from osteitis deformans
Should be differentiated from the localized vertebral lipping associated with collapse
or fibrosis of an intervertebral disk, called spondylosis and from the traction spurs
that may follow localized injury of an intervertebral articulation.
TREATMENT
Rest and restriction of activity
Salicylates are useful in relieving discomfort
Obesity should be corrected by dietary measures
A well-fitted back support helpful in controlling pain and in preventing recurrent
attacks
2. Osteoarthritis of the Hip

ETIOLOGY
Unknown
Trauma associated with incongruity of the joint surfaces is thought to be an
important factor in secondary OA
Also often a late sequel of congenital dysplasia of hip, reduced congenital dislocation
or congenital coxa vara
It often appears many years after an epiphyseal disturbance such as slipping of the
capital femoral epiphysis
Osteonecrosis of the femoral head is likely to result in distortion of the articular
surface, leading sooner or later to OA of the hip.
INCIDENCE
Less frequent in Chinese patients than in age-matched white populations
PATHOMECHANISM
Begin in areas of the femoral had not subject to weight bearing pressure are
fibrillation, erosion, and thinning of the articular cartilage.
The cartilage becomes irregularly worn away over the head and in the acetabulum
and the exposed bone becomes hard and eburnated. Proliferation of osteophytes in
the form of a collar converting the spherical joint to a form nearly cylindrical and this
proliferation selectively limits rotation and abduction-adduction movements of the
hip while relatively preserving flexion and extension.
The acetabulum grows larger as the head of femur flattens and its femoral neck may
become short and broad.
In addition to spurring and gross changes of contour roentgenograms show
narrowing of the cartilage space, irregular areas of increased bone density, mottling
of head and neck and numerous cyst like near the articular surfaces.
The synovial membrane also usually becomes thick and fibrous.
SIGNS AND SYMPTOMS

Stiffness and pain.
People affected with hip osteoarthritis often find it difficult to bend or move around.
DIAGNOSIS
Roentgenographic findings
History and clinical signs
Differential Diagnosis
Ischemic necrosis of the femoral head, RA, tuberculosis, neuropathic joint disease
and subacute or late forms of pyogenic arthritis may simulate OA of the hip.
TREATMENT
Medical
1. General Measures weight reduction by low calorie diet when the patient is obese
and regulation of physical activity to ensure adequate rest from prolonged weight
bearing . For limited periods analgesic medications may be indicated.
2. Local nonsurgical treatment The use of heat is often helpful and also active, non
weight bearing exercises of the hip should be carried out daily in an effort to preserve
range of motion.
3. Surgical treatment operation is indicated if the patients pain is intolerable
By arthroplasty both pain and stiffness in the osteoarthritic hip can often be
satisfactorily. Total hip arthroplasty is the most effective method of relieving pain
and restoring movement.
Hemiarthroplasty the femoral side of the hip joint is replaced by a prosthesis, is

usually not indicated in OA, because both sides of the joint are involved by the
disease.
Arthrodesis provides complete and permanent relief of hip pain, it is often the
operation choice for young.
Trochanteric osteotomy the pain of the hip OA can often be partially relieved
through this.
DRUG THERAPY
Acetaminophen
Oral NSAIDs
Tramadol
Intra-articular corticosteroid injections
3. Osteoarthritis in the Knee
Most common form of arthritis in the knee
Degenerative,"wear-and-tear" type of arthritis that occurs most often in people 50
years of age and older, but may occur in younger people too
Osteoarthritis develops slowly and the pain it causes worsens over time
SIGNS AND SYMPTOMS

Stiffness, pain, and swelling
Difficulty in walking, climbing, sitting on the chair or getting up after sitting for
some time
TREATMENT
Strengthening exercises for quadriceps and hamstring mm (early stage)
Weight reduction in obese patients and limitation of the patients activities
Hot compress, rest and elastic knee support for acute pain and swelling
Minimize activities that aggravate the condition, such as climbing stairs
Switching from high impact activities (like jogging or tennis) to lower impact
activities (like swimming or cycling) will put less stress on your knee
Losing weight can reduce stress on the knee joint, resulting in less pain and increased
function
Using devices such as a cane, wearing shock-absorbing shoes or inserts, or wearing a
brace or knee sleeve can be helpful. A brace assists with stability and function, and
may be especially helpful if the arthritis is centered on one side of the knee.
DRUG THERAPY
Acetaminophen
Oral NSAIDs
Topical NSAIDs
Tramadol
Intra-articular corticosteroid injections
SERONEGATIVE ARTHROPATHIES
I-II DEFINITION OF TERMS

SPONDYLOARTHROPATHIES
Ankylo- bent
Spondylos- vertebral disk
ANKYLOSING SPONDYLITIS
Enthesopathy- swelling of Achilles tendon at its insertion
Anterior uveitis inflammation of at any point of the pigmented layer of the eyeball
known as uveal tract
HLA-B27 Human Leukocyte Antigen B-27; 95%; proteins found on the surface of
WBC; cause WBC to attack the body
Sacroiliitis inflammation of one or both sacroiliac joints
INCIDENCE
There is no adequate evidence that the incidence of AS has changed in the last few
decades
Clinical features, age of onset, and survival time have remained stable
One study revealed an overall age and gender-adjusted incidence of 7.3 per 100,000
person-years. This U.S. figure compares quite well with the Finnish study, which
revealed a stable incidence of 8.7 (95% confidence interval [CI] 6.4 to 11.0) per
100,000 people aged 16 or older.
Gradual onset
Frequent in men
20-40 y.o.
III. ETIOLOGY
Genetics
HLA-B27
PATHOMECHANISM
Chronic Inflammatory Disease
Systemic disorder
Affects the spine primarily the sacroiliac joint
Ascending involvement of the spine
Progress in cephalad direction
Intermittent bouts of back pain that may radiate into the buttocks
Back pain worse in the morning
Stiffness for hours that improve with activity
Back motions become limited
Normal lumbar back curve flattened
Thoracic curvature exaggerated
Chest expansion is limited
Entire spine becomes fused
Enthesopathy (hallmark)
Anterior uveitis
Spondylitic heart disease- atroventricular conduction defects and aortic regurgitation
Fatigue
Anorexia
Weight loss
Anemia
ESR (Erythrocyte Sedimentation Rate)
Serologic tests for rheumatoid factor
Anti-CCP antibodies are negative
HLA-B27 MRI- detects earliest radiographic changes in SI joint
PT Evaluation
Maintain joint ROM
Postural training
Prone push up on elbows
Back extension swimming
VI. TREATMENT
Medical
NSAIDS first line treatment
Slow radiographic progression of spinal disease
Reduce pain and suppress joint inflammation and muscle spasm
TNF Inhibitors- NSAID-resistant axial disease
For symptoms that are refractory to NSAIDS:
Etanercept- 50g subcutaneously once a week
Adalimumab- 40mg subcutaneously every other week
Infliximab- 5mg/kg every other month by intravenous infusion
Sulfasalazine- 1000 mg orally twice a day
PT
Modified Schobers Test
1. Feet width apart
2. Mark the central point between PSIS
3. Mark 5cm below et 10cm above
4. Keep knees straight
5. Bend forward to touch toes
6. Measure the length of the marks (15- the length when bending)
(-) above 5cm difference
(+) less than 5cm
Lumbar Spine Side Flexion Test

1. Heels against the wall
2. Feet width apart
3. Back against the wall
4. Measure distance from mid finger to the foot (both sides)
5. Side flex to side
6. Avoid rotation
Re-measure (+) unequal measurement
PSORIATIC ARTHRITIS

Osteolysis
Oligoarticular
Onycholysis
Psoriasis
Syndesmophyte- bony growth attached to a ligament
III. ETIOLOGY
PATHOMECHANISM
Causes asymmetric sacroiliitis and syndesmophytes

Symmetric polyarthritis
Oligoarticular form that may lead to considerable destruction of the affected joints
Pattern of disease in which the DIP joints are primarily affected
Pitting of nails and onycholysis frequently accompany DIP involvement
Severe deforming arthritis in which osteolysis is marked
Spondylitic form in which sacroiliitis and spinal involvement predominate
Sausage swelling of the digits
Patch of psoriasis in the scalp, gluteal cleft or umbilicus
Chronic Inflammation of the joints closest to the tips of the fingers and toes,
sometimes hips knee and spine
Back pain
ESR
High Uric acid levels
PT EVALUATION
TREATMENT
Medical
NSAIDs mild cases
Methotrexate- 7.5-20mg orally once a week; for pts that doesnt respond to NSAIDs;
improve cutaneous and arthritic manifestations
TNF Inhibitors- for disease that are refractory to methotrexate
Corticosteroids- less effective; may precipitate postural psoriasis during tapers
Antimalarials- exacerbate psoriasis
REACTIVE ARTHRITIS

Balanitis- swelling of the foreskin and head of the penis
Stomatitis- inflammation of the mouth and lips
Keratoderma blennorrhagicum- skin lesion commonly found on the palms and soles
Conjunctivitis mild, transient and easily missed
Anterior uveitis Carditis- inflammation of the heart
Aortic regurgitation diastolic flow of blood from the aorta into the LV
Achilles tendonitis- inflammation of the Achilles tendon
III. ETIOLOGY
Sexually transmitted-men (20-40 y.o.)
Genital infections with Chlamydia trachomatis or Ureaplasma urealyticum are most
often implicated
Dysenteric- both genders; from Shigella, Salmonella, Yersinia or Campylobacter
PATHOMECHANISM
Develops within 1-4 weeks after a gastrointestinal infection
Asymmetric
Involves weight-bearing joints

Fever
Sausage digit and toe
Weight loss
Balanitis
Stomatitis
Keratoderma blennorrhagicum
Conjunctivitis mild, transient and easily missed
Anterior uveitis
Carditis Aortic regurgitation
Achilles tendonitis
Gonococcal Arthritis - initially mimic reactive arthritis, but the marked improvement
after 24-48 hours of antibiotic administration and the culture results distinguish the
two disorders
Gouty Arthritis
Psoriatic Arthritis
Rheumathoid Arthritis
Behcet disease - may also mimic reactive arthritis
HLA-B27 ESR- check for inflammation
C- reactive protein- check inflammation
Synovial fluid analysis- look infection for joints
Chlamydia test- look for evidence of infection by Chlamydia Trochoatis
Stool culture- look for Salmonella, Campylobacter, E. coli, yersinia
VI.TREATMENT
Medical
NSAIDs- mainstay of therapy
Antibiotics- nongonobobbal sexually transmitted infection; for chronic reactive
arthritis (6mos)
Sulfasalazine- 1000mg orally twice a day
Methotrexate- 7.5- 20 mg orally per week
TNF agents- recent-onset disease that is refractory to NSAIDs
CRYSTAL INDUCED ARTHROPATHIES

Commonly seen arthropathies:
Calcium pyrophosphate Acute pseudogout; A variety dihydrate (CPPD) of chronic
inflammatory or degenerative arthritis; Chondrocalcinosis
Basic calcium phosphate Calcific periarthritis; Hydroxy- apatite (BCP)
Acute/Chronic inflammatory arthritis; Destructive arthropathy; Soft-tissue calcinosis
Monosodium Urate (MSU) Acute/chronic gouty arthritis; Renal calculi; Tophi
Uncommon arthropathies:
Calcium oxalate aluminium Acute arthritis in patients phosphate on renal dialysis
Cholesterol Chronic synovial effusions in RA/OA
Xanthine Acute arthritis (rare); Renal calculi; Asymptomatic deposition in muscles
Cysteine/cystine Acute arthritis
Charcot-Leyden Synovial fluid and tissues, (lysophospho-lipase) with eosinophilia
Calcium pyrophosphate dihydrate (CPPD) and Basic calcium phosphate hydroxy-
apatite (BCP)- are the common calcium containing crystals that can result in a
variety of joint symptoms due to their deposition in and around joints.
Pseudo-gout- an acute attack of synovitis caused by the crystals
Chondrocalcinosis- fine layer of calcification overlying the menisci and articular
cartilage of the knee
Calcific periarthritis- acute inflammatory attacks of arthritis, usually around the
shoulder, caused by BCP crystals
INCIDENCE
More common in men, the attack typically lasts from a few days to 3-4 weeks and
is characterised by acute pain, swelling and warmth at the affected joint, often
indistinguishable from gout.
Attacks may be precipitated by any intercurrent illness, recent surgery or trauma and
rapid diuresis.
Pseudorheumatoid arthritis is seen in less than 5% of all CPPD patients. It is also
called CPPD disease type B. This is associated with a sub-acute inflammatory
polyarthritis, which may persist for a few months and therefore may mimic RA.
Pseudo-osteoarthritis accounts for about 50% of CPPD patients. It is also referred to
as CPPD disease types C & D. Type C differs from type D, in that acute attacks are
superimposed on the more chronic symptoms, whereas in type D, there are no acute
attacks of joint pain.
Pseudoneuropathic also referred to as type F CPPD disease, is rare. It has been
described in tertiary syphilis and severe neurotrophic arthritis.
III. ETIOLOGY
Calcium Crystal Induced Inflammation
Calcium pyrophosphate dihydrate (CPPD) and basic calcium phosphate hydroxy-
apatite (BCP), are the common calcium containing crystals that can result in a variety
of joint symptoms due to their deposition in and around joints.
CPPD crystals may be deposited in fibrous and articular cartilage. The crystals may
provoke an acute attack of synovitis- referred to as pseudo-gout. The deposits are
often visible as a fine layer of calcification overlying the menisci and articular
cartilage of the knee- termed chondrocalcinosis
BCP crystals can also cause acute inflammatory attacks of arthritis, usually around
the shoulder, referred to as calcific periarthritis.
Calcium pyrophosphate dihydrate (CPPD) crystal associated arthropathies

CPPD crystal deposition disease is usually idiopathic and presents as sporadic
episodes in the majority of patients.
There are rare familial forms of the disease and an association with some metabolic
disorders- such as hyperparathyroidism, haemochromatosis, hypophosphatasia,
Wilsons disease, ochronosis, hypo-calciuric hypercalcaemia (and perhaps other
hypercalcaemic states), diabetes mellitus and hypomagnasaemia- has been
documented.
Treatment of osteoarthritis (OA) of the knee with intra-articular injections of
hyaluronic acid preparations (such as Hylan GF-20) has also been associated with
triggering of an acute attack of pseudo-gout.
PATHOMECHANISM
Familial CPPD deposition disease may present in one of two ways:
1. First as a rather benign, early onset (< 50 yrs), usually acute presentation, having a
polyarticular distribution involving the knee, wrist, shoulder, elbow, hip or ankle and
recurrent episodes of crystal-positive acute pseudo-gout and chondrocalcinosis.
2. The second a more chronic arthropathy, with a late onset (> 50 yrs), destructive oligo/
mono-arthropathy, affecting the knees, wrists, shoulders or hips. Thus CPPD crystal
associated disease is clinically heterogeneous and may cause both an acute or chronic
arthritis.
Pseudogout is the most common form (also called CPPD disease type A) and
presents as acute episodes of synovitis at a single joint, most often at the knee.

May cause median nerve compression at the wrist
May cause spinal canal stenosis due to involvement of the ligamentum flavum
May even cause a cervical spine myelopathy.
Acute gouty arthritis must be distinguished from other causes of acute mono-
arthritis, such as infective (septic) arthritis; traumatic synovitis; palindromic
rheumatism or palindromic onset rheumatoid arthritis; the sero-negative spond-
arthritides, such as psoriatic arthritis or spondarthritis with peripheral joint synovitis,
or sarcoid arthritis.
Chronic tophaceous gout may be confused with nodular rheumatoid arthritis
Acute gout; an acute inflammatory arthritis (synovitis); which may be associated
with tenosynovitis; bursitis; and/or cellulitis.
The distinguishing features of CPPD disease type B from RA, would be:
The presence of degenerative (OA) features
Absence of typical marginal erosions on x-rays of the hands or feet
Presence of chondrocalcinosis and/or typical CPPD crystals on the synovial fluid
examination
Absence of rheumatoid factor
Silent and asymptomatic
Usually diagnosed by the presence of chondrocalcinosis, detected by radiology
There are fairly marked degenerative changes on radiology of the affected joint(s) in
addition to chondrocalcinosis
VI. TREATMENT
Medical
NSAIDs - The first line of therapy is to rest the affected joint and to use full doses of
a non-steroidal anti-inflammatory drug (NSAID). The NSAIDs that are of particular
benefit in this situation, are indomethacin 50mg 8 hrly (or maximum 50mg 6 hrly);
naproxen 500mg 12 hrly; ketoprofen or flurbiprofen 100mg 8 hrly; or diclofenac
50mg 8 hrly.
Colchicine can be a useful adjunct to NSAIDs if the acute attack does not settle
rapidly. In a dose of 0.5 mg twice or three times a day, one can avoid the GI side
effects seen with higher doses of colchicine and still obtain added therapeutic benefit.
Intravenous colchicines has been reported to be very effective in treating acute gout
and some rheumatologists advocate this as the treatment of choice.
Steroids - Most acute attacks respond satisfactorily to either full doses of an NSAID,
or to the combination of an NSAID and low dose colchicine, as described above.
Occasionally, the clinical response may not be as rapid as desired, or it may prove
necessary to aspirate the affected joint for diagnostic synovial fluid analysis. In either
situation, injecting the affected joint with steroid (methyl-prednisolone or
triamcinalone) may prove to be extremely useful in rapidly resolving the synovitis.
Intra-articular steroid can also be very useful in situations where NSAID use is
contra-indicated, either due to GI intolerance or renal involvement. It is also
extremely important to remember that allopurinol or uricosuric drugs should not be
commenced during an acute attack of gout. These drugs should be initiated only after
satisfactory resolution of the acute attack and on adequate colchicine/NSAID
prophylactic cover.
SYSTEMIC LUPUS ERYTHEMATOSUS (SLE)
I-II . DEFENITION OF TERMS

Systemic Lupus Erythematosus A chronic, systemic, inflammatory disease
characterized by injury to the skin, joints, kidneys, heart and blood-forming
organs, nervous system, and mucous membranes.
Lupus Nephritis kidney inflammation caused by SLE.
Lupus Panniculitis clinically characterized by erythematous deep nodules
involving the upper extremities and face
Discoid lupus a limited form of the disease confined to the skin presenting as
coin-shaped lesions, which are raised and scaly
Systemic Lupus usually more severe than discoid lupus and can affect almost
any organ or system of the body
Vasculitis inflammation of blood or lymph vessel
Mesenteric vasculitis inflammation of the mesenteric vasculature. Most often
this involves medium-sized branches of the celiac, superior mesenteric, and
inferior mesenteric arteries.
Arthralgia pain in one or more joints
Myositis inflammation and degeneration of muscle tissue
Osteonecrosis death of bone cells due to decreased blood flow
Serositis Inflammation of the serous tissues of the body (the tissues that line the
lungs, heart, abdomen, and inner abdominal organs).
Hemolytic anemia anemia due to the destruction, rather than underproduction,
of red blood cells
Reticulocytosis - An elevation in the number of reticulocytes (young red blood
cells) in blood, a sign of unusually rapid red blood cell production.
Leukopenia a shortage of white blood cells
Lymphopenia a reduction in the numbers of lymphocytes in the blood
Thrombocytopenia (low platelet count) refers to a decreased number of platelets
in the blood
Alopecia hair loss
Organic brain syndrome Psychiatric or neurological symptoms that arise from
damage to or disease in the brain. Also known as organic mental disorder.
INCIDENCE
The incidence of SLE is influenced by many factors, including gender, race, and genetic
inheritance.
1. Malar Rash Fixed erythema, flat or raised, over the malar eminences,
tending to spare the nasolabial folds
2. Discoid Rash Erythematous raised patches with adherent keratotic
scaling and follicular plugging; atrophic scarring may
3. Photosensitivity occur in older lesions
Skin rash as a result of unusual reaction to sunlight, by
4. Oral Ulcers patient history or physician observation
Oral or nasopharyngeal ulceration, usually painless,
5. Arthritis observed by a physician
Nonerosive arthritis involving two or more peripheral
6. Serositis joints, characterized by tenderness, swelling, or effusion
a) Pleuritis: convincing history of pleuritic pain or
evidence of pleural effusion
7. Renal disorder b) Pericarditis: documented by ECG, evidence of
pericardial effusion
a) Persistent proteinuria
8. Neurologic disorder b) Cellular casts (a cast having a hyaline or waxy matrix
with inclusion of cells), which may be red cell,
9. Hematologic disorder hemoglobin, granular, tubular, or mixed
Seizures and psychosis: in the absence of offending drugs
or known metabolic derangements
a) Hemolytic anemia with reticulocytosis
10. Immunologic disorder b) Leukopenia
c) Lymphopenia
d) Thrombocytopenia
11. Antinuclear antibody a) Anti-DNA: antibody to native DNA in abnormal titer
b) Anti-Sm: presence of antibody to Sm nuclear antigen
c) Positive finding of antiphospholipid
An abnormal titer of antinuclear antibody (ANA) by
immunofluorescence or an equivalent assay at any point
in time and in the absence of drugs known to be
associated with drug-induced lupus syndrome
SLE can occur at any age, but it is most common in persons between the ages of 15 and
40 years old.
Women are affected 10 to 15 times more often than men.
Sex hormones appear to play some role; most cases develop after menarche
and before menopause.
Among older individuals, the gender distribution is more equal.
Race is also a factor, as SLE occurs in 1:1000 white women but in 1:250 black
women.
SLE is more common in African-American, African-Caribbean, Hispanic-
American, and Asian persons than in Caucasian population.
Familial occurrence of SLE has been repeatedly documented, and the disorder
is concordant in 25-70% of identical twins. If a mother has SLE, her
daughters risks of developing the disease are 1:40 and her sons risks are
1:250.
Aggregation of serologic abnormalities (positive antinuclear body) is seen in
asymptomatic family members, and the prevalence of other rheumatic
diseases is increased among close relatives of patients.
CLASSIFICATION
A person must have SLE if any four or more of the 11 criteria are present, serially or
simultaneously, during any interval of observation
III.ETIOLOGY
The exact cause of SLE is unknown, although it appears to result from an
immunoregulatory disturbance brought about by the interplay of genetic, hormonal,
chemical, and environmental factors.
Some of the environmental factors that may trigger the disease are infections (e.g.,
Epstein-Barr virus), antibiotics (especially those in the sulfa and penicillin groups),
exposure to UV light, and extreme physical and emotional stress, including
pregnancy.
PATHOMECHANISM
Interaction among various genetic and environmental factors, multiple genes, sex,
and hormonal milieu contribute to disease susceptibility; eventually will result to
immune dysregulation.
The activation of B and T cells requires stimulation by specific antigens.
Both professional APCs and B cells process the antigen into peptides and present
them to T cells through their surface HLA molecules. The activated T cells in turn
stimulate the B cells to produce pathogenic autoantibodies.
The increased rate of apoptosis would increase the chance of leakage of intracellular
antigens that may either trigger an autoimmune response or participate in the
formation of immune complexes.
Under normal circumstances, apoptotic cells are engulfed by macrophages in the
early phase of apoptotic cell death without inducing inflammation or the immune
response. Recent studies have shown that the clearance of apoptotic cells by
macrophages in patients with SLE is impaired.
It could be the result of quantitative or qualitative defects of the early complement
proteins, such a C2, C4, or C1q.
The C1q receptors on the surface of phagocytes constitute an extremely important
mechanism for the clearance of apoptotic cells.
C1q deficiency develop antibodies and a lupus-like syndrome apparently because of
the inability to eliminate apoptotic cells effectively, which leads to an increase in the
exposure of antigens to the immune system.
Loss of immune tolerance
The total number of peripheral blood T cells is usually reduced, probably because of
the effects of anti-lymphocyte antibodies.
IV.SIGNS AND SYMPTOMS
Constitutional symptoms (especially low-grade fever and fatigue)
Achy joints (arthralgia)
Arthritis (swollen joints)
Arthralgia
Skin rashes (malar)
Pulmonary involvement (e.g., pleurisy, pleural effusion: chest pain, difficulty
breathing, cough)
Anemia
Kidney involvement (e.g., lupus nephritis)
Sun or light sensitivity (photosensitivity)
Alopecia
Raynauds phenomenon (fingers turning white or blue in the cold)
CNS involvement:
Seizures
Headache
Peripheral neuropathy
Cranial neuropathy
Cerebral vascular accidents
Organic brain syndrome
Psychosis
Mouth, nose, or vaginal ulcers
Sjogren syndrome (SS)
- It is strongly linked to lymphoma. SS patients do not commonly
exhibit photosensitivity even though anti Ro antibodies circulate in
their blood. It does not respond to hydroxychloroquine.
Fibromyalgia (FM)
- It does not cause inflammation, arthritis, skin rashes, or damage to
tissues, organs and bones like lupus. Medications commonly used to
treat lupus have little or no effect on the symptoms of FM.
Scleroderma
- Defined by thickened and hardened skin, usually on the fingers but
also on the hands, feet, forearms, and face. It results from an
overproduction of collagen, a connective tissue present throughout the
body and a component of scar tissue.
Rheumatoid Arthritis
- RA is not fatal but attacks joints, primarily the fingers, wrists, knees,
and ankles.
- It can also cause joints to deform. It can cause bone erosion and
deformity.
A patient referred for incidental positive ANA should have a careful history and
physical examination to look for clinical findings of SLE. Not all patients with a
positive ANA have SLE or a connective tissue disease. Two percent to 5% of healthy
persons carry a low to moderate positive ANA. On the other hand, if there is a
clinical suspicion of SLE, a detailed workup should be initiated with appropriate
blood tests, urine tests, x-rays, and other studies that may be required based on the
presentation. In an outpatient setting, most rheumatologists order a white blood cell
count (WBC) with differential, comprehensive metabolic panel (CMP), erythrocyte
sedimentation rate (ESR), C-reactive protein (CRP), ANA panel, Smith, RNP, SSA
and SSB, complements C3 and C4, dsDNA, and a urine analysis. Most
rheumatologists also screen their patients for tuberculosis, hepatitis, thyroid diseases,
and pregnancy, because a positive test affects the choice of immunosuppression and
future follow-up.
It is also worthwhile to check for APLAs (lupus anticoagulant, cardiolipin antibodies,
and 2 microglobulin) because SLE and APLA commonly coexist and are often
found together in patients with prior thrombotic events or frequent miscarriages.
If one suspects primary Sjogren's syndrome, rheumatoid factor (RF), cryoglobulin
levels, and 2 microglobulins should be checked. Primary Sjogren's syndrome
patients tend to have a positive ANA, rheumatoid factor, and SSA or SSB.
Occasionally these patients have sicca symptoms and negative laboratory results, in
which case a lip biopsy with a focus score is required to prove or disprove the
diagnosis of primary Sjogren's syndrome. Sjogren's syndrome, however, can also be
secondary to any underlying connective tissue disease, especially SLE and
rheumatoid arthritis.
Other diagnostic tests are ordered as indicated and consist of joint x-rays and chest x-
ray; renal ultrasound; CT scans of the chest, abdomen, and pelvis; echocardiograms;
CT angiograms; electromyography and nerve conduction tests; neuropsychiatric
testing; vascular studies; and biopsies of the skin, kidneys, nerves, and lungs.
VI.TREATMENT
Medical
Minor joint symptoms can usually be alleviated by rest and NSAIDs.
Antimalarials (hydroxychloroquine) may be helpful in treating lupus rashes or joint
symptoms and appear to reduce the incidence of severe disease flares.
Corticosteroids are required for the control of certain complications. The lowest dose
that controls the condition should be used.
Centranervous system lupus may require higher doses of corticosteroids than are
usually given.
Treatment of severe lupus nephritis included an induction phase and a maintenance
phase.
Cyclophosphamide has been for many years the standard treatment for both phases
of lupus nephritis.
Mycophenolate mofetil appears to be an effective alternative treatment.
When cyclophosphamide is required, gonadotropin-releasing hormone analogs can
be given to protect a woman against the risk of premature ovarian failure.
For patients with the antiphospholipid syndrome, anticoagulation is the treatment of
choice.
Pregnant patients with recurrent fetal loss associated with antiphospholipid
antibodies should be treated with low-molecular-weight heparin plus aspirin.
Therapies targeted specifically to the treatment of joint manifestations.
PROGRESSIVE SYSTEMIC SCLEROSIS

Progressive Systemic Sclerosis
Autoimmune d/o
Characterized by inflammation & fibrosis of many parts of the body including skin,
blood vessels, synovium, skeletal muscles & certain internal organs such as kidneys,
lungs, heart & GI tract
a.k.a Scleroderma
Progresses slowly
Derived from the Greekword for hard skin & emphasizes the dermatological
component of the disease
INCIDENCE
3 to 4 times more common in females than in males especially between the ages of
30 and 50.
Peak of incidence of occurrence is in 50 to 60 years old.
About 30% of patients with scleroderma die within 5 years of onset due to infection
or by kidney or heart failure
9 year survival rate in scleroderma averages approximately 40%
Breast and lung CA may be common
Atrophy & deformity with scleroderma are MC in childhood
Diffuse systemic sclerosis (dSSc) occurs more often in black women than in white
women
CLASSIFICATION
1. Limited scleroderma
80% of patients
a.k.a CREST syndrome (Calcinosis cutis, Raynauds phenomenon, Esophageal
motility d/o, Sclerodactyly & Telangiectasia)
Often characterized by a long history of Raynauds phenomenon before the
development of other symptoms
Skin thickening is limited to the hands frequently with digital ulcers & to the face
Esophageal dysmotility (common)
Milder than diffused scleroderma
Life threatening complications can occur from SI involvement & pulmonary
hypertension
2. Diffused scleroderma
20% of patients
More acute onset with many constitutional symptoms, arthritis, carpal tunnel
syndrome and marked swelling of the hands & legs
Widespread skin thickening occurs, progressing from fingers to trunk
Internal organ problems including GI effects & pulmonary fibrosis (common)
Severe life-threatening involvement of the heart & kidney occurs
III. ETIOLOGY
The underlying etiology is generally unknown but there are some possible causes that
includes:
Anticancer agents such as bleomycin (Blenoxane) or nonopoid analgesics such as
pentazocine (Talwin)
Fibrosis due to an abnormal immune system response
Systemic exposure to silica dust or polyvinyl chloride
Underlying vascular cause with tissue changes initiated by persistent perfusion
Genetic factors
PATHOMECHANISM
1. Usually begins in the fingers & extends proximally to the upper arms, shoulders, neck
and face.
2. The skin atrophies, edema and infiltrates containing CD4 T cells surrounding the blood
vessels & inflamed collagen fibers become edematous (losing strength & elasticity) and
degenerative.
3. The dermis becomes tightly bound to the underlying structures resulting in atrophy of
the affected dermal appendages & destruction of the distal phalanges by osteoporosis.
4. As the disease progresses, this atrophy can affect other areas.
E.g. Some muscles & joints become fibrotic
5. Complications include compromised circulation due to abnormal thickening of the
arterial intima possibly causing slowly healing ulcerations on fingertips or toes leading to
gangrene.
6. Patient may also experience decreased food intake & wt loss as a result of GI
symptoms, arrhythmias & dyspnea due to cardiac & pulmonary fibrosis & malignant
hypertension due to renal involvement called renal crisis.

SKIN
Raynauds phenomenon & tight skin (hallmarks)
Patients with dSSc have taut skin in the more proximal parts of extremities in
addition to the thorax & abdomen; early features also include polyarthralgia, wt loss
& malaise
Patients with lSSc have patchy skin changes with teardrop-like appearance known as
morphea
Skin tightening of SSc beings on the fingers & hands in nearly all cases
Cutaneous disease usually develop before visceral involvement & can manifest
initially as non-pitting subcutaneous edema associated with pruritus
Telangiectasia, pigmentation & depigmentation
Ulcerations of the fingertips & subcutaneous calcifications are seen
Taut, shiny skin over the entire hand & forearm due to skin thickening
Tight & inelastic facial skin causing a masklike appearance & pinching of the mouth;
contractures with progressive tightening
MUSCULOSKELETAL
Articular complaints (common)
Pain, stiffness & swelling of fingers & joints
Muscle involvement is usually mild with weakness, tenderness and pain of proximal
muscles of the upper & lower extremities
Muscle atrophy, muscle weakness, deconditioning & flexion contractures (late
symptoms)
VISCERA
Esophageal hypomotility
Intermittent diarrhea, bloating, cramping, malabsorption & wt loss
Interstitial pulmonary fibrosis
Cardiac involvement such as cardiomyopathy, pericarditis, pericardial effusions or
arrhythmias
Scleroderma can cause diagnostic confusion with other causes of Raynauds
phenomenon particularly SLE (systemic lupus erythematosus), mixed connective
tissue disease & inflammatory myopathies.
It can be mistake for other d/o characterized by skin hardening like Eosinophilic
fasciitis
Diseases that have similar characteristics to PSSc:
Eosinophilic fasciitis - a rare d/o presenting with skin changes that resemble dSSc
but the inflammatory abnormalities are limited to the fascia rather than the dermis &
epidermis, presence of peripheral blood eosinophilia, absence of Raynauds
phenomenon, good response to prednisone & association with paraproteinemias
Scleromyxedema - diffused skin thickening & visceral involvement, presence of
paraprotein, absence of Raynauds phenomenon & distinct skin histology
Diabetic cheiropathy - develops in long-standing, poorly controlled diabetes & can
mimic sclerodactyly
Nephrogenic fibrosing dermopathy - produces thickening & hardening of the skin of
the trunk and extremities of patients with renal failure
Laboratory test results reveals slightly elevated erythrocyte sedimentation rate, (+)
rheumatoid factor 23% to 35% of patients & (+) antinuclear antibody
Urinalysis shows proteinuria, microscopic hematuria & casts
Hand x-rays reveal terminal phalangeal tuft resorption, subcutaneous calcification &
joint space narrowing & erosion
Chest x-rays show bilateral basilar pulmonary fibrosis
GI x-rays reveal distal esophageal hypomobility & stricture, duodenal loop dilation,
small bowel malabsorption pattern & large diverticula
Pulmonary function studies show decreased diffusion & vital capacity
Electrocardiogram shows nonspecific abnormalities related to myocardial fibrosis
Skin biopsy reveals changes consistent with disease progression such as thickening
of the dermis & occlusive vessel changes
PT Evaluations
To maintain function & promote muscle strength, heat therapy to relieve joint
stiffness & patient teaching to make performance of daily activities easier
ROM exercises; stretching program for fingers; moving the face by exaggerated
facial expressions, manual stretching of the mouth with thumbs & oral exercises with
the use of a tongue depressor
VI. TREATMENT
Medical
Immunosuppresants (e.g. Cyclosporine or chlorambucil)
Vasodilators & antihypertensives, digital sympathectomy or rarely cervical
sympathetic blockade to treat Raynauds phenomenon
Antacids, omeprazole, proton pump inhibitor, periodic dilation & soft bland diet for
esophagitis with stricture
Broad spectrum antibiotics to treat small bowel involvements to counteract the
bacterial growth in the duodenum & jejunum related to hypomotility
ACE inhibitor to preserve renal function
PT
Parrafin wax bath
1. Soak the patients hand in the wax bath.
2. Remove the hand & cover it with plastic or cling wrap.
3. Use cloth to cover plastic and let it stay there for about 20 minutes.
4. Remove the cloth, plastic and wax.
5. Instruct the patient to play with the wax by moving his fingers.
Finger exercises (self exercise)

1. Practice making a fist and then stretching all your fingers like a star.
2. Touch each one of your finger tips with your thumb tip.
3. With your hands face down on a table, lift each finger up in turn.
Blocking exercises for fingers (self exercise)

1. Using a block work the individual finger joints by blocking off before the end crease,
actively bend the end of the finger & assist with the other hand to gain full bend.
Straighten out fully, assist if necessary.
2. Repeat with the block placed before the second crease.
3. Repeat with the block placed before the third crease (in the palm of the hand).
Face exercises (self exercise)
Stretches should be held for at least 10 seconds & performed 3x a day
1. Lift the eyebrows then lower them.
2. Squeeze your eyes tightly. Wink tightly with either eye.
3. Frown your forehead to wrinkle the bridge of your nose, raise your upper lip to
increase the stretch.
4. Flare your nostrils. Close your lips hard.
5. Cover your teeth with your lips and then open your mouth as wide as you can.
6. Bare your teeth & open the mouth as far as you can. Push the jaw forward to produce
an underbite.
7. Grin as widely as you can without showing the teeth.
Massage
1. Put lubricant on patients extremity
2. Use effleurage for about 10 - 20 minutes
3. Proceed to cross friction massage & continue for 5 - 10 minutes
4. Finish off with compression massage which lasts for another 10 - 15 minutes
Aerobic exercises
Do gentle cardiovascular or aerobic exercises regularly for at least 20 - 30 minutes, 4 5
times a week.
E.g. Swimming, dog walking, aqua aerobics, gardening, cycling
REFERENCES
Overview: Anatomy and Physiology
Physical Rehabilitation (Fifth Edition), S. OSullivan, T. Schmitz
Physical and Medical Rehabilitation: Principles and Practice, J. DeLis
Understanding Arthritis and Rheumatism, M. I.V. Jayson, MD, A.St.J. Dixon M
Principles of Anatomy and Physiology 13th Edition G. Tortora, B. Derrickson
Juvenile Rheumatoid Arthritis

Understanding Diseases by Lippincott Williams and Wilkin
Professional guide to diseases by Lippincott Williams and Wilkin
Essentials of Pathophysiology second edition concepts of altered health states by Carol
Mattson Porth
http://www.spineuniverse.com/conditions/spinal-arthritis/jra/types-juvenile-rheumatoid-
arthritis
http://www.webmd.com/rheumatoid-arthritis/understanding-juvenile-rheumatoid-
arthritis-basic
http://www.patient.co.uk/doctor/juvenile-idiopathic-arthritis-pro
Osteoarthritis
Handbook of Orthopaedic Surgery Tenth Edition by H. Robert Brashear Jr. and R. Beverly
Raney Sr.
Physical Rehabilitation Fifth Edition by Susan B. O Sullivan and Thomas J. Schmitz
http://www.healthpages.org/health-a-z/osteoarthritis-degenerative-joint-disease/
http://emedicine.medscape.com/article/330487-overview
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2920533/
http://www.orthop.washington.edu/?q=patient-care/articles/hip/osteoarthritis-of-the-hip-
hip-arthritis.html
http://orthoinfo.aaos.org/topic.cfm?topic=a00212
Seronegative Arthropathies
Current Medical Diagnosis and treatment 52bd edition by Maxine A. Papadakis and Stephen
J. Mcphee.Copy right 2013 by Mcgraw-hill Companies,inc.
Delisas Physical Medicine and Rehabilitation Principles and Practice 5 th Edition vol.1 copy
right 2010 by Lippuncott Williams & Wilkins,Philadelphia.
Journal of the royal society o medicine vol.76 June,1983
Mercks.com
Crystal Induced Arthropathies

Practitioner Series: J Indian Rheumatol Assoc 2002 : 10 : 5 - 13 S J Gupta
Consultant Physician & Rheumatologist, Apollo Indraprastha & Sant Parmanand Hospitals,
New Delhi.
Systemic Lupus Erythematosus

Goodman, C.C., Snyder, T.E. 2009. Differential Diagnosis for Physical Therapists:
Screening for Referral, 4th Edition. Singapore: Elsevier Pte Ltd.
Chan, L., Harrast, M.A., Kowalske, K.J., Matthews, D.J., Ragnarsson, K.T., Stolp, K.A. 2011.
Physical Medicine and Rehabilitation, 4th Edition. Singapore: Elsevier Pte Ltd.
Firestein, G.S., Budd R.C., Harris E. Jr., McInnes, I.B., Ruddy, S., Sergent, J.S. 2008. Kelleys
th
Textbook of Rheumatology, 8 Edition. Philadelphia: W.B. Saunders Company
Papadakis, M.A., McPhee, S.J. 2013. Current Medical Diagnosis and Treatment, 52 nd Edition.
United States: The McGraw-Hill Companies, Inc.
Wright, B., Bharadwaj, S. 2010. The Cleveland Clinic Foundation. [Online]. Available:
http://www.clevelandclinicmeded.com/medicalpubs/diseasemanagement/r
heumatology/systemic-lupus-erythematosus/. [7 July 2014].
Progressive Systemic Sclerosis

Differential Diagnosis for Physical Therapists by Goodman & Snyder
Current Medical Diagnosis & Treatment 2009 by Stephen J. McPhee & Maxine A. Papadakis
Lippincott Manual of Nursing Practice Series, Pathophysiology. Lippincott Williams &
Wilkins. By Gary J. Arnold, MD et al.
Professional guide to signs & symptoms (4th edition) by Peggy. D Baikie et al.
Introduction to Massage Therapy by Mary Beth Braun
http://www.patient.co.uk/doctor/systemic-sclerosis-scleroderma
http://www.sclerodermasociety.co.uk/userfiles/leaflets/Physiopherapy.pdf
http://www.rightdiagnosis.com/s/scleroderma_systemic/treatments.htm
http://www.medscape.com/viewarticle/717087_2
http://www.physiopedia.com/Cross_friction_massage
http://www.sclerodermatt.org/articles/better-health/414-scleroderma-and-massage-
therapy

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PAUL UNIVERSITY ILOILO

Leader: Esther Marie Sazon (Adult Rheumatoid Arthritis)

July 11, 2014

OVERVIEW: ANATOMY AND PHYSIOLOGY

The structural classification of joints is based on two criteria:

IV. SIGNS AND SYMPTOMS

I-II. DEFINITION OF TERMS:

IV. SIGNS AND SYMPTOMS

I-II. DEFINITION OF TERMS

IV. SIGNS AND SYMPTOMS

2. Osteoarthritis of the Hip

SIGNS AND SYMPTOMS

Hemiarthroplasty the femoral side of the hip joint is replaced by a prosthesis, is

SIGNS AND SYMPTOMS

I-II DEFINITION OF TERMS

Lumbar Spine Side Flexion Test

I-II. DEFINITION OF TERMS

IV. SIGNS AND SYMPTOMS

I-II. DEFINITION OF TERMS

IV. SIGNS AND SYMPTOMS

I-II. DEFINITION OF TERMS

Calcium pyrophosphate dihydrate (CPPD) crystal associated arthropathies

IV. SIGNS AND SYMPTOMS

I-II . DEFENITION OF TERMS

I-II. DEFINITION OF TERMS

IV. SIGNS AND SYMPTOMS

Finger exercises (self exercise)

Blocking exercises for fingers (self exercise)

Juvenile Rheumatoid Arthritis

Crystal Induced Arthropathies

Systemic Lupus Erythematosus

Progressive Systemic Sclerosis

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