cfmopd arthritis

8/2/2019 Cfmopd Arthritis

1/22

ARTHRITIS

Jennilyn Bancifra and Bernadette M. Cid

CFM JI April-May 2012


2/22

OSTEOARTHRITIS

caused by the breakdown and eventual loss of

the cartilage of one or more joints

a.k.a DEGENERATIVE JOINT DISEASE; occurs

more frequently as a person ages


3/22

osteoarthritis


4/22

OSTEOARTHRITIS

Commonly affects

hands, feet, spine and

large weight bearing

joints such as hips andknees

Primary vs. Secondary


5/22

Causes of Primary OA

Age

Degeneration of the protein content of thecartilage

Repetitive use of joints Incites irritation and inflammation of the cartilage

Inflammation of cartilage

Stimulates new bone growths (spurs) Hereditary

Can be found in multiple members of the family


6/22

Causes of Secondary OA

Obesity

Trauma or surgery to joint structures

Congenital abnormalities Diabetes and other hormone disorders


7/22

Symptoms

Pain on affected joint/s after repetitive use

Usually more severe later in the day

In complete loss of cartilage, pain may be present

even at rest or with limited motion

Swelling, warmth and creaking of joints

Stiffness of joints after prolonged inactivity

Intermittent

No systemic symptoms


8/22

Symptoms

OA of the kneeBow Legged Deformity

Limping

Irritation of spinal nerves from bony spurs ofan arthritic spine numbness, tingling, pain


9/22

Symptoms

HEBERDENS NODE

Bony enlargements at

the distal

interphalengeal joint

From bone spurs

May not be painful but

may limit motion


10/22

Symptoms

Bouchards Node

Bony enlargements at

the proximal

interphalangeal joint

Also may not be painful

but may limit motion


11/22

Diagnosis

Osteoarthritis Gout Rheumatoid

Arthritis1

Key presenting

symptoms

Pauciarticular. Pain

with movement,improving with rest.

Site of old injury

(sport, trauma).

Obesity. Occupation.

Monoarticular.

Abrupt onset. Pain atrest and movement.

Precipitating event

(meal, physical

stress). Family history.

Polyarticular. Gradual,

symmetricinvolvement. Morning

stiffness. Hands and

feet initially involved

more than large

joints. Fatigue, poorly

restorative sleep.


12/22

DiagnosisOsteoarthritis Gout Rheumatoid

Arthritis

Key physical findings Infrequent warmth,

effusion. Crepitus.

Enlargement/spur

formation.

Malalignment.

Podagra. Swelling,

warmth. Exquisite

pain with movement.

Single joint

(exceptionsplantarfascia, lumbar spine).

Tophi.

Symmetric swelling,

tenderness. MCP,

MTP, wrist, ankle

usually before larger,

proximal joints.Rheumatoid nodules.

Key laboratory, x-ray

findings

Few characteristic

(early). Loss of joint

space, spurformation,

malalignment (late).

Synovial fluid with

uric acid crystals.

Elevated serum uricacid. 24 h urine uric

acid.

Elevated ESR/CRP.

Rheumatoid factor.

Anemia of chronicdisease. Early

erosions on x-ray,

osteopenia at

involved joints.


13/22

Treatment

Goals of Treatment

Relief of Pain

Restoration of Function

Reduction of Disease Progression


14/22

Treatment

Pain Medications (NSAIDs, Capsaicin,

Glucosamine+ Chondroitin)

Physical Therapy

Assistive devices

Intraarticular injections

Surgery


15/22

NON-STEROIDAL ANTI-INFLAMMATORY

DRUGS FOR THE TREATMENT OF PAIN

AND IMMOBILITY-ASSOCIATED

OSTEOARTHRITIS: CONSENSUS

GUIDANCE FOR PRIMARY CARE

Adebajo, Ade (2012), BMC Family Practice


16/22

ABSTRACT

Osteoarthritis is a common presentation in

primary care, and non-selective non-steroidal

anti-inflammatory drugs (sometimes also

referred to as traditional NSAIDs or tNSAIDs) andselective cyclo-oxygenase 2 inhibitors (COX-2

inhibitors) are commonly used to treat it.


17/22

ABSTRACT

The UK's National Institute for Health and

Clinical Excellence (NICE) recommends taking

patient risk factors into account when selecting

a tNSAID or a COX-2 inhibitor, but GPs havelacked practical guidance on assessing patient

risk.


18/22

METHODS

Developing an evidence-based consensus

statement with an accompanying flowchart

that aimed at providing concise and specific

guidance on NSAID use in osteoarthritistreatment


19/22

RESULTS

1. tNSAIDs are effective drugs in relieving pain and

immobility associated with osteoarthritis. COX-2

inhibitors are equally effective

2. tNSAIDs and COX-2 inhibitors vary in theirpotential gastrointestinal, liver, and cardio-renal

toxicity. This risk varies between individual

treatments within both groups and is increasedwith dose and duration of treatment


20/22

RESULTS

3. COX-2 inhibitors are associated with a

significantly lower gastrointestinal toxicity

compared to tNSAIDs. Co-prescribing of aspirin

reduces this advantage.

4. PPIs should always be considered with a

tNSAID and with a COX-2 inhibitor in higher GI

risk patients. An accompanying flowchart toguide management was also agreed.


21/22


22/22

CONCLUSION

Ascertaining individual patient risk is

important when choosing treatment for

patients with osteoarthritis.

cfmopd arthritis

Documents