ARTHRITIC

Review of Anatomy &

Physiology
of a
JOINT
JOINTS
 JOINT
CLASSIFICATION
Structural Classification of
Joints

• Fibrous Joints

• Cartilaginous joints

• Synovial joints
FIBROUS JOINTS
CARTILAGINOUS JOINT
SYNOVIAL JOINTS
Functional Classification of
Joints

• Synarthrosis

• Amphiarthrosis

• Diarthrosis
 Structural
Classification of
Joints
3 Types of Fibrous
Joints
3 Types of Fibrous Joints

I. Sutures
3 Types of Fibrous Joints

II. Syndesmoses
 3 Types of Fibrous Joints

III. Interosseous
Membranes
 2 Types of
Cartilaginous Joints
2 Types of Cartilaginous Joints

•Synchondrosis
 2 Types of Cartilaginous Joints

• Symphysis
Structure of a Typical Synovial
Joint
6 Types of Synovial
Joints
6 Types of Synovial Joints

• Plane joints
6 Types of Synovial Joints

• Hinge joints
6 Types of Synovial Joints

• Pivot joints
6 Types of Synovial Joints

• Condyloid joints
6 Types of Synovial Joints

• Saddle joints
6 Types of Synovial Joints

• Ball-and-Socket Joints
 Rheumatoid arthritis (RA)

• is a systemic
rheumatic
disease
characterized
by an acute
inflammatory
response
CLASSIFICATION

Adult Juvenile
Rheumatoid
Rheumatoid Arthritis
ETIOLOGY of Adult Rheumatoid
Arthritis

• unknown
• Theories:
 Immunogenetic
 Infectious disease or viral
 Combination of both
PATHOMECHANISM

• Grossly edematous appearance of the

synovium with slender villous
• Hair-like projections in the joint cavity
• Distinctive vascular changes
 venous distention
 capillary obstruction
 neutrophilic infiltration of the arterial walls
 areas of thrombosis and hemorrhage
Pannus formation
SIGNS AND SYMPTOMS

• Morning stiffness
• Muscle atrophy around affected joints.
• Anorexia, weight loss, and fatigue
• Marked by a bilateral and symmetrical
pattern of joint involvement.
• Presence of immobility and the
cardinal signs of inflammation.
SIGNS AND SYMPTOMS

• Joint pain or Arthralgia

• Crepitus
• Restricted movement
• Development of nodules
• Tenosynovitis
Many disorders can simulate RA:
• RF can be nonspecific and is often present in
several autoimmune diseases
• Some patients with crystal-induced arthritis may
meet criteria for RA;
• Systemic Lupus Erythematosus
• Sarcoidosis, Whipple disease, multicentric
reticulohistiocytosis, and other systemic diseases
may involve joints.
• Reactive arthritis
• Psoriatic
• Osteoarthritis
SYSTEMIC LUPUS ERYTHEMATOSUS
SARCOIDOSIS
WHIPPLE DISEASE
MULTICENTRIC
RETICULOHISTIOCYTOSIS
PSORIATIC
 ANCILLARY PROCEDURES

• Elevated erythrocyte
sedimentation rate (ESR) or C
reactive protein (CRP)
ANCILLARY PROCEDUREs

• Complete blood count (CBC)

ANCILLARY PROCEDUREs

• Synovial fluid analysis

ANCILLARY PROCEDUREs

• Radiographic study
PT EVALUATION

• patient history and relate

that problem to the
patient’s past medical
history
• signs and symptoms
• previous level of activity
• current medication
PT EVALUATION

• Range of motion
• Strength
• Joint stability
• Endurance
• Functional examination
• Gait and mobility
• Sensory integrity
• Psychological status
• Environmental barriers
TREATMENT
I. Medical

• Nonsteroidal anti-inflammatory drugs (NSAIDs)

• Disease-modifying antirheumatic drugs

(DMARDs)

• Corticosteroids

• Surgical treatment for RA

II. PT

• Modalities for pain relief

• Superficial heat:
• moist hot packs
• dry heating pads and
lamps
• paraffin
• hydrotherapy.
MOIST HOT PACKS
PARAFFIN
II. PT

• Local application of cold will also produce local

analgesia and increase in superficial circulation at
the site.
• Patients must be encouraged to perform self-ROM
to the extent possible to maintain motion.
• Therapists are also to let the patient perform
isometric exercise and dynamic exercise
• Therapists should also target functional activities
that require specific techniques of joint
protection.
• Endurance and functional training
JUVENILE RHEUMATOID
ARTHRITIS
JUVENILE RHEUMATOID
ARTHRITIS

• “Juvenile Idiopathic Arthritis”

• Affecting children younger than age 16
• an inflammatory disorder of the
connective tissues
• joint swelling and pain or tenderness
Three Major Types

• Systemic

• Polyarticular

• Pauciarticular
Systemic

• Often called as “Still’s disease”

• Affect internal organs:
• Heart
• Liver
• Spleen
• lymph nodes.
• Child may experience mild, transient arthritis or
frank poly-arthritis associated with fever and
rash.
SYSTEMIC JUVENILE RA
 SYSTEMIC

• Symptoms usually
subside in 6 to 12
mos.
• Child’s behavior
may clearly suggest
joint pain and
fatigue.
• Initial appearance
in adulthood.
 POLYARTICULAR

• 30% of all children are

affected

• Affects five or more

joints during the the first
6 mos.
POLYARTICULAR

• Most commonly involved: SMALL JOINTS

• Symmetrical: 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)
• Affects: LARGE JOINTS
• Most likely to develop: Girls under age 8
PAUCIARTICULAR

• Affects two distinct groups

1. Girls younger than 6 years of age with

chronic uveitis

2. Late-onset arthritis (mostly boys)

ETIOLOGY

• Unknown
• Possible genetic factors or an abnormal
immune response
• Viral or bacterial (particularly
streptococcal) infection
• Trauma
• Emotional stress
PATHOMECHANISM

• 4 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
SIGNS AND SYMPTOMS
SYSTEMIC JRA

• joint pain • Lymphadenopathy

• rheumatoid rash • Myocarditis
• Fever • Nonspecific
• Hepatosplenomegaly abdominal pain
• Irritability • Pericarditis
• Listlessness • Pleuritis
POLYARTICULAR JRA

•Developmental •Hepatosplenomegaly
retardation •Listlessness
•Hepatosplenomegaly •Low-grade fever with
•Listlessness daily peaks
•Low-grade fever with •Lymphadenopathy
daily peaks
POLYARTICULAR JRA

•Lymphadenopathy
•Subcutaneous nodules on the elbow
•Swollen
•Stiff
•Developmental retardation
•Tender joints
•Weight loss
HEPATHOSPLENOMEGALY
LYMPHADENOPATHY
PAUCIARTICULAR
CHRONIC IRIDOCYCLITIS

• CHRONIC IRIDOCYCLITIS
• asymptomatic inflammation of the iris and ciliary
body
• SACROILIITIS
• Sacroiliac and lumbar arthritis characteristic of
ankylosing spondylitis
• JOINT INVOLVEMENT BUT NEGATIVE FOR ANAs
and HLA-B27 and WITHOUT IRITIS
• Asymmetrical involvement of large or small joints
CHRONIC IRIDOCYCLITIS
SACROILIITIS
DIFFERENTIAL DIAGNOSIS

• Leukemia

• Septic Arthritis

• Systemic Lupus Erythmatosus (SLE)

• Juvenile Dermatomyositis
Septic Arthritis
Juvenile Dermatomyositis
ANCILLARY PROCEDURES

• Complete Blood Count

• Erythrocyte
Sedimentation Rate

• Positive HLA-B27 test

• X-ray
PT EVAL

• 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
TREATMENT
I. Medical

• Non-Steroidal Inflammatory Drugs

(NSAIDs)
• Disease-Modifying Antirheumatic
Disease (DMARDs)
• Systemic steroids
• Corticosteroids and Mydriatics
• Surgery
II. 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
(DEGENERATIVE JOINT
DISEASE)
Osteoarthritis

• chronic arthritis
• middle aged and elderly people
• weight bearing joints
• degenerative changes in articular
cartilages
• bony overgrowth at the joint margins.
Etiology

• OA is obscure
• Aging
• Trauma
• Remodelling of bone
• Repetitive Microtrauma
• repetitive KNEE BENDING
• Obesity
 Secondary
Primary Osteoarthritis Osteoarthritis
• no underlying cause • an antecedent disease
for the joint disease or injury related to
is clearly apparent the arthritis may
result from any
condition that disturbs
normal joint function
• frequently seen in a
younger age
Pathomechanism

• cartilage seems to lose some of its ability to

withstand mechanical stresses
• swelling of the chondrocytes
• chondromucoid softening of the matrix.
• 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
 Pathomechanism

• EARLY STAGES
• increased production of protein
polysaccharide by proliferating cartilage
cells in the deeper layers , perhaps as a
compensation for the matrix loss
• Late stages
• Underlying bone may be denuded
• mild inflammatory reaction
• synovial membrane and periarticular tissues
thickened
SIGNS AND SYMPTOMS

• STIFFNESS of one or more joints

• ACHING PAIN
• SLIGHT ENLARGEMENT OF THE AFFECTED
JOINTS
• limitation of joint motion
• pain (joint is at rest)
• Crepitation
• Fatigue
Diagnosis

• Plain radiography
• In the load-bearing areas, radiographs can depict
joint-space loss, as well as subchondral bony
sclerosis and cyst formation

• Computed tomography (CT) scanning

• used in the diagnosis of malalignment of the
patellofemoral joint or of the foot and ankle
joints
Diagnosis

• Magnetic resonance imaging (MRI)

• can directly visualize articular cartilage and other joint
tissues (e.g., meniscus, tendon, muscle, or effusion)

• Ultrasonography
• tool for monitoring cartilage degeneration

• Bone scanning
• Helpful in the early diagnosis of osteoarthritis of the hand;
can also help differentiate osteoarthritis from osteomyelitis
and bone metastases
PT EVAL

• review the chart

• patient history
• identifying the signs and symptoms
• a review of the cardiopulmonary,
integumentary, and neuromuscular
systems.
PT should also examined the
patient’s:

• Range of Motion
• Strength
• Joint Stability
• Endurance
• Functional Examination
• Mobility and Gait
• Sensory Integrity
• Psychological Status
• Environmental Barriers
Ancillary Procedures

• Rheumatoid factor (RF) and Cyclic

citrullinated peptide antibody (CCP)
• Synovial fluid analysis
• Erythrocyte sedimentation rate (sed
rate or ESR
• C-reactive protein (CRP)
• Complete blood count (CBC)
• Comprehensive metabolic panel (CMP
TREATMENT

For Osteoarthritis
I. Medical

• General measures
• Drug therapy
• Local treatment of joints
• Prevention of deformity
• Surgical measures
II. PT

• Modalities for Pain Relief

• Joint Mobility
• Strengthening
• Endurance Training
• Functional Training
• Gait training
• Education
 
CLASSFICATIONS OF OSTEOARTHRITIS

1. Osteoarthritis of the Spine

2. Osteoarthritis of the Hip
3. Osteoarthritis in the Knee
1. Osteoarthritis of the spine
• Extremely common
• Seen most often in stocky and obese
persons over 40 years of age
• More frequent in males than females
• Often observed in the lumbar and
cervical levels 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

• roentgenographics changes of lippins

• spurs and irregular bone formation about the
vertebral margins
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

• Unknown (etiology)
• 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
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
PATHOMECHANISM

• 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

For Osteoarthritis of the Spine

I. Medical

• General Measures
• Local nonsurgical treatment
• Surgical treatment
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
• 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
• Hot compress, rest and elastic knee support
• Minimize activities
• Switching from high impact activities to lower impact
activities
• Losing weight can reduce stress on the knee joint
• Using devices such as a cane, wearing shock-absorbing
shoes or inserts, or wearing a brace or knee sleeve can
be helpful
DRUG THERAPY

 Acetaminophen
 Oral NSAIDs
 Topical NSAIDs
 Tramadol
 Intra-articular corticosteroid injections
SERONEGATIVE ARTHROPATHIES
CONDITIONS

• ANKYLOSING SPONDYLITIS
• PSORIATIC ARTHRITIS
• REACTIVE ARTHRITIS
ANKYLOSING SPONDYLITIS

“Stiff Spine”

• A.K.A :
MARIE STRUMPELL DISEASE
BEKHSTEREV’S DISEASE
ETIOLOGY

• GENES
PATHOMECHANISM

• Begins in the sacroiliac joints

Progress upwards and can involve the entire spine

Shoulders and hips involved

SIGNS AND SYMPTOMS

• intermittent bouts of back pain that may

radiate into the buttocks
• back pain
• stiffness
• back motions become limited
• normal lumbar back curve flattened
• thoracic curvature exaggerated
• chest expansion is limited
SIGNS AND SYMPTOMS

• entire spine becomes fused

• Enthesopathy
• Anterior uveitis
• Fatigue
• Weight loss
ANCILLARY PROCEDURES

• ESR

• Anti-CCP antibodies are negative

• HLA-B27 positive

• MRI

• X-RAY
PT Evaluation

• Chest Expansion Test

• Modified Schober’s Test

• Lumbar Spine Side Flexion Test

TREATMENT
I. Medical

• NSAID
• TNF Inhibitors- NSAID-resistant axial disease
II. PT

• POSTURE CORRECTION
sleeping-?
Sitting-?

• Joint mobilization
• Breathing exercises
• use of modalities for pain relief
• Swimming
PSORIATIC ARTHRITIS
Etiology

• GENETIC FACTOR

• ENVIRONMENT
Trauma
Bacteria
Classifications

• Asymmetric mono/oligoarthritis
• Symmetric polyarthritis
• DIP involvement
• Arthritis Mutilans
PATHOMECHANISM

• Causes
asymmetric
sacroiliitis and
syndesmophytes
SIGNS AND SYMPTOMS

• 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
SIGNS AND SYMPTOMS

• 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
DIFFERENTIAL DIAGNOSIS

RHEUMATOID ARTHRITIS ANKYLOSING SPONDYLITIS

Symmetric Strong HLA B27 association

PIP, MCP Dominant in males

Ulnar deviation, swan neck Axial involvement

deformities

Rheumatoid nodules Bamboo spine

ANCILLARY PROCEDURES

• ESR
• Rheumatoid Factor negative
• ACPA negative
• X-ray
TREATMENT
I. Medical

• NSAIDs
• Methotrexate
• TNF Inhibitors
• Corticosteroids
• Antimalarials-
II. PT

• Exercises:
passive et active stretching et strengthening

• Modalities

• Orthotics
REACTIVE ARTHRITIS
ETIOLOGY

• Sexually transmitted
-Genital infections with Chlamydia
trachomatis or Ureaplasma urealyticum are
most often implicated

• Dysenteric- from Shigella, Salmonella, Yersinia

or Campylobacter
 
PATHOMECHANISM

• Develops within 1-4 weeks after a

gastrointestinal infection

• involves weight-bearing joints

SIGNS AND SYMPTOMS

• Fever
• Sausage digit and toe
• Weight loss
• Balanitis
• Stomatitis
SIGNS AND SYMPTOMS

• Keratoderma blennorrhagicum
• Conjunctivitis mild, transient and easily
missed
• Anterior uveitis
• Carditis Aortic regurgitation
• Achilles tendinitis
KERATODERMA BLENNORRHAGICUM
BALANITIS
CONJUNCTIVITIS
STOMATITIS
ANTERIOR UVEITIS CARDITIS
AORTIC REGURGITATION
ACHILLES TENDONITIS
DIFFERENTIAL DIAGNOSIS

• Gonococcal Arthritis
• Gouty Arthritis
• Psoriatic Arthritis
• Rheumathoid Arthritis
• Behcet disease
ANCILLARY PROCEDURES

• HLA-B27

• ESR

• C- reactive protein

• Synovial fluid analysis

• Chlamydia test

• Stool culture
 TREATMENT

For REACTIVE ARTHRITIS

I. Medical

• NSAIDs
• Antibiotics
• Sulfasalazine
• Methotrexate
• TNF agents
II. PT

• Wrist splints
• Ice packs et hot packs

• Relaxation exercises
• Hydrotherapy
CRYSTAL INDUCED ARTHROPATHIES
DEFINITION OF TERMS

• Commonly seen arthropathies

• Calcium pyrophosphate Acute pseudogout

• Basic calcium phosphate Calcific

periarthritis

• Monosodium Urate (MSU) Acute/chronic

gouty arthritis
DEFINITION OF TERMS

• Uncommon arthropathies:
• Calcium oxalate aluminium Acute arthritis
• Cholesterol Chronic synovial effusions in RA/OA
• Xanthine Acute arthritis (rare)
• Cysteine/cystine Acute arthritis
• Charcot-Leyden Synovial fluid and tissues
• Calcium pyrophosphate dihydrate (CPPD)
• Pseudo-gout
• Chondrocalcinosis
• Calcific periarthritis
ETIOLOGY

• Calcium Crystal Induced Inflammation

• Calcium pyrophosphate dihydrate

(CPPD) crystal associated arthropathies
PATHOMECHANISM

• 1. First as a rather begin, 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.
SIGNS AND SYMPTOMS

• median nerve compression

• spinal canal stenosis

• cervical spine myelopathy

DIFFERENTIAL DIAGNOSIS

• Acute gouty arthritis

• Chronic tophaceous gout
• Acute gout
ANCILLARY PROCEDURES

• 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
 TREATMENT

For CRYSTAL INDUCED ARTHROPATHIES

I. Medical

• NSAIDs
• Colchicine
• Steroids
SYSTEMIC LUPUS
ERYTHEMATOSUS (SLE)
Definition of Terms

• Systemic Lupus Erythematosus

• Lupus Nephritis
• Lupus Panniculitis
• Discoid lupus
• Systemic Lupus
• Vasculitis
Definition of Terms

• Mesenteric vasculitis
• Arthralgia
• Myositis
• Osteonecrosis
• Serositis
• Hemolytic anemia
Definition of Terms

• Reticulocytosis
• Leukopenia
• Lymphopenia
• Thrombocytopenia
• Alopecia
• Organic brain syndrome
Lupus Panniculitis
Discoid lupus
Vasculitis
Osteonecrosis
Alopecia
ETIOLOGY

• unknown
• 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.
• 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.
PATHOMECHANISM

• The increased rate of apoptosis would increase

the chance of leakage of intracellular antigens
that may either trigger an autoimmune response
• Apoptotic cells are engulfed by macrophages in
the early phase of apoptotic cell death without
inducing inflammation or the immune response.
• It could be the result of quantitative or
qualitative defects of the early complement
proteins, such a C2, C4, or C1q.
PATHOMECHANISM

• 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
SIGNS AND SYMPTOMS

• Constitutional symptoms (especially low-grade

fever and fatigue)
• Achy joints (arthralgia)
• Arthritis (swollen joints)
• Arthralgia
• Skin rashes (malar)
SIGNS AND SYMPTOMS

• 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
SIGNS AND SYMPTOMS

• Raynaud’s 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
DIFFERENTIAL DIAGNOSIS

• Sjogren syndrome (SS)

• Fibromyalgia (FM)

• Scleroderma

• Rheumatoid Arthritis
ANCILLARY PROCEDURES

• white blood cell count (WBC) with differential

• comprehensive metabolic panel (CMP)
• erythrocyte sedimentation rate (ESR)
• C-reactive protein (CRP)
• ANA panel
• Smith test for lupus
• RNP
• SSA and SSB complements C3 and C4
• dsDNA and a urine analysis
ANCILLARY PROCEDURES

• OTHERS
• 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
• biopsies of the skin, kidneys, nerves, and lungs
TREATMENT

For SLE
I. MEDICAL

• rest and NSAIDs (for minor joint symptoms)

• Antimalarials
• Corticosteroids
• Cyclophosphamide
• Mycophenolate mofetil (effective alternative
treatment)
• Anticoagulation
• low-molecular-weight heparin plus aspirin (for
pregnant pt)
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
• Greekword for “hard skin”
CLASSIFICATION

• Limited scleroderma (80% of pt)

CLASSIFICATION

• Diffused scleroderma (20% of pt)

ETIOLOGY

• Unknown
• Some possible cause:
• 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
• 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.
PATHOMECHANISM

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
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.
SIGNS AND SYMPTOMS
• SKIN
• Raynaud’s phenomenon &
tight skin (hallmarks)
• Taut skin in the more
proximal parts of extremities
in addition to the thorax &
abdomen
• Patchy skin changes with
teardrop-like appearance
known as morphea
• Skin tightening(fingers &
hands)
• 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
• Non-pitting subcutaneous
edema associated with
pruritus
SIGNS AND SYMPTOMS

• 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)
SIGNS AND SYMPTOMS

• VISCERA
• Esophageal hypomotility
• Intermittent diarrhea, bloating, cramping,
malabsorption & wt loss
• Interstitial pulmonary fibrosis
• Cardiac involvement such as
cardiomyopathy, pericarditis, pericardial
effusions or arrhythmias
DIFFERENTIAL DIAGNOSIS

• Scleroderma
• Eosinophilic fasciitis
Diseases that have similar
characteristics to PSSc:

Eosinophilic fasciitis
Diseases that have similar
characteristics to PSSc:
Scleromyxedema
Diseases that have similar
characteristics to PSSc:

Diabetic cheiropathy
Diseases that have similar
characteristics to PSSc:
Nephrogenic fibrosing dermopathy
ANCILLARY PROCEDURES

• Urinalysis
• Hand x-rays
• Chest x-rays
• GI x-rays
• Pulmonary function
• Electrocardiogram
• Skin biopsy
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
 TREATMENT

For PROGRESSIVE SYSTEMIC SCLEROSIS

I. Medical

• Immunosuppresants (e.g. Cyclosporine or chlorambucil)

• Vasodilators & antihypertensives, digital
sympathectomy or rarely cervical sympathetic blockade
to treat Raynaud’s 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
I. PT

• Parrafin wax bath

• Finger exercises (self exercise) 
• Blocking exercises for fingers (self exercise)
• Face exercises (self exercise)
• Massage
• Aerobic exercises
END…