1 sem!

IS A CONDITION OF JOINTS WHERE THERE IS PAIN AND/OR SWELLING.

ARTHRITISARTHRO means “JOINT” and –ITIS means “INFLAMMATION”

“Inflammation of the joint”

Most important determinants in classifying arthritis:

INFLAMMATORY or NON-INFLAMMATORYSYMMETRICAL or NONSYMMETRICAL

SYSTEMIC or NON-SYSTEMIC MANISFESTATION

CLASSIFICATION OF ARTHRITIS DSE.

Rheumatoid Arthritis (RA)- synovial membrane

(structure between 2 bones forming the joints)

Distal joints

(hands and feet)

BILATERAL

Elderly and obese

Pain is experience when the joints are moved after prolong sitting/standing

2 MAJOR FORMSOsteoarthritis (OA)-articulating portion of the bone

Weight-bearing joints-(hips, knee, spine)

NOT BILATERAL

No particular age group

OA

•Pain occurs usually in the afternoon

•No swelling

•Weakness & atrophy of muscles

RA

•Painful even at rest & usually in the morning

•Swelling

•Areas around the joints are warm

•Weakness and atrophy of muscles

Typical Signs and symptoms

systemic autoimmune, connective tissue disorder of unknown etiology that primarily affect the synovial

lining of diarthrodial joint.

RHEUMATOID ARTHRITIS

Universal and found in all population (possible genetic/environmental factors)

RA affects women 2 or 3 times often more than men in typical years of onset between ages 20-60. Men equally affected as women over the age 65 appear.

Men with RA past 60 y/o typically present without stiffness and swelling in UE.

Elderly over 50s had features of Polymyalgia rheumatica (characterized by pain in shoulder & pelvic girdle muscles, eleveted ESR & absence of muscle dse)

Dse onset is usually insidious with complaints of gen. jt.pain & stiffness.

Acute onset is seen 8-15% of RA px

RA Epidemiology

UNKNOWN etiology.Current research into the causes of RA is based on a complex,

but as yet incomplete, appreciation of the functions of the immune system.

Briefly, antigen is a substance, usually foreign to the host, which provoke the immune system into action. The immune system may respond to the antigen directly (cellular immunity) or by the production of antibodies that circulate in the serum (humoral immunity).

These responses involve two general kinds of lymphocytes: T cells, which are responsible for cellular immunity, and B cells, which produce circulating antibodies specific to the antigen. Antibodies are immunoglobulins, a type of serum protein.

RA is said to be an AUTOIMMUNE disorder.

RA etiology

It is not clear wheter the abN immune response is a primary event or is a response to specific antigen from any external stimulus.

Proposed Theory includes:a. Abberant fxning of cell mediated immunity &

defective T-lymphocytesb. Bacterial organismsc. Viral etiologyd. Rheumatoid factors (antibodies against IgG)e. Genetic predisposition demonstrated by Human

Leukocytes Antigen

RA etiology

Long standing RA is characterized by grossly edematous appearance of the synovium with slender villous or hair-like projection in the jt. cavity

Vascular changes: including venous distention, capillary obstruction, neutrophilic infiltration of arterial walls& areas of thrombosis & hemorrhage.

PANNUS – synovial proliferation of vascular granulation tissue; it dissolve collagen as it extends over the jt. Cartilage.

Granulation will result in adhesion & fibrous or bony ankylosis of the jt.

Chronic inflammation weakens the jt. Capsule & ligaments altering the jt. structure & fxn.

Ruptured tendons and fraying of tendon sheaths produce imbalance in the muscle pull resulting to deformities.

RA pathology

Proteases, collagenase & cathepsin cause synovium to proliferate & become inflamed. They also cause cartilage & bone destruction by pannus formation.

Immune complexes are stored in articular cartilage, because of lack of limiting membrane between the jt. Spaces & synovial blood vessels. The storage causes chronic inflammatory responses.

RA pathogenesis

Rheumatoid Arthritis

Systemic manifestations:-HALLMARK SYMPTOM OF RA: morning stiffness lasting more

than 3 mins.- Difficulty moving up & generalized stiffness despite morning

activity hepl to differentiate stiffness from DJD- Anorexia, fever, weightloss, fatigue

Muscle involvement-Atrophy around the joints may be present early- Muscle weakness d/t reflex inhibition 2* to pain or atrophy

Tendons-Tenosynovitis-Lag phenomenon

RA signs and symptoms

Specific Jt. Involvement:-marked by bilateral symmetrical pattern involvement.- immobility and the cardinal signs of inflammation: pain, redness, swelling, and

heat. I- arthralgia is used to refer to pain in ajoint. - crepitus , which is audible or palpable grating or crunching a the joint i moved

through it range of motion (ROM). Crepitus is the result of uneven degeneration of the jt. Surface

ATLANTOAXIAL & MIDCERVICAL REGION – most common site of inflammation DIP JOINTS- most uninvolved joint in RA KNEES – one of the most frequently affected joints

COMMONLY AFFECTED JOINTS: CERVICAL, TMJ, SHOULDER, ELBOW,WRIST, HAND JOINTS (mcp, pip, dip, thumb), HIP JOINTS, KNEES, ANKLES AND FEET

RA signs and symptoms

Rheumatoid Arthritis

Rheumatoid nodules

Vascular complication

Neurologic manifestations

Cardiopulmonary complication

Ocular manifestation

RA secondary complications

Is a condition marked by 2 features:

a. DESTRUCTION of articular cartilage

b. FORMATION of new bone at the margins of the joint

OSTEOARTHRITIS

The most common arthritis is an assymentrical non-inflammatory dse. that has no systemic components.

3 types:PRIMARYSECONDARYEROSIVE INFLAMMATORY

HALLMARK of the dse: Cartilage degeneration

Osteoarthritis

No single factor has been identified.

Aging strongly associated with OA

Factors r/t to aging contributes to OA

Trauma

Occupational tasks

Obesity

Etiology

OA pathologyFirst OA change in articular cartilage is an

increase in water contentThe increase suggest proteoglycans to swell

with water beyond normalMechanism is unknownLater stage: proteoglycans are lost which

deminish water content of cartilageCollagen synthesis increaseAs articular cartilage is destroyed, joint space

narrows.

OA pathogenesisMajor pathological changes of OA are found

in articular cartilage (concentration of proteoglycan)

Met changes in rate of enzyme production facilitate the destruction of cartilage

Proteoglycan & collagen synthesis increases until late stages of the disease.

Women are more commonly have OA of small joints – DIP, PIP, MCP, & 1st MTP, 1st CMC jts.

Men – often have hip involvement

OA epidemiology

1. Primary OA – spares the shoulder & elbow, except in secondary OA

Decreasing frequency:knee – first MTP – 1st CMC – hips – cervical spine –

lumbar spine

2. Secondary OA – caused by an injury, fx, occupation-related task or obesity

3. Erosive inflammatory – common in middle aged women

3 types of OA

The main impact of OA on fxn result from involvement of large weight-bearing jts., which can cause pain & limit mobility.

Back involvement ranks next.

OA of hand is not assoc with significant impairment in ADL, except when there is significanmt OA of the CMC joint of the thumb.

OA

Monoarticular involvementNo symmentric signs and symptomsStiffness may be experienced upon

awakening or after a period of rest or inactivity. NOT IN THE ENTIRE BODY AS RA.

Pain in the joint – primary reason for physical limitations; worsen in motion but not at rest (except late stage)

KELLGREN’s SYNDROME – generalized OA

OA signs and symptoms

Pain in OA is attributed to:

-incongruent articulation to jt surface-periosteal elevation-abN pressure on subchondral bone-trabecular microfx-distention of jt capsule

OA signs and symptoms

Specific Joint involvement:HIP, KNEE, FOOT, CMC

OA signs and symptoms

Deformed joints

Difficulty in doing day-to-day activities

(ex: walking)

Tightness of joints

Complications

Program Therapy for Persons with

Arthritis

To relieve or reduce painTo maintain the integrity of joints

To prevent further deformities of the joints

To strengthen the muscles around the joints

Goals

Modalities for pain reliefJoint mobilityStrengtheningJoint protectionFunctional trainingGait trainingEducation

PT INTERVENTION

When there is swelling Hot pack application (20 minutes for 15 day) Comfortable joint position without causing

deformity

When there is less pain Move joints as tolerated by PWD

What will also help?1. Good nutrition2. Reduction of weight for obese3. Cane usage

Treatment Procedures

Thank you for listening!

© Abby Girl Carasi Ocado Cecille Anne Cayetano, BSPT4