SLE

Disease of unknown etiology in which tissues and

cells undergo damage mediated by tissue binding
auto-antibodies and immune complex.

Genetic, environmental, and sex hormonal factors

are likely of pathogenic importance.

T and B cell hyperactivity, production of autoantibodies with specificity for nuclear antigenic
determinants, and abnormalities of T cell function
occurs.

Clinical Manifestations:

90% are women

Child bearing age

common in blacks than in whites

Characterized by periods of
exacerbation and remissions.

May involve virtually any organ system

and have a wide range of disease
severity.

Common Features:

fever, fatigue, malaise, weight loss

Rashes( butterfly), photosensitivity,

vasculitis, alopecia, oral ulcers.

arthritis- inflammatory, systemic, nonerosive.

anemia, neutropenia,
thrombocytopenia, lymphadenopathy,
splenomegaly

pericarditis, pleuritis, myocarditis,

endocarditis

Nephritis, peritonitis, seizures,

psychosis.

Drug- Induced Lupus

Induced by drugs such as procainamide,

isoniazid, hydralazine, chlorpromazine,
methyldopa, minocycline, anti TNF agents.

Features are predominantly constitutional, joint

and pleurocardial.

All patients have antinuclear antibodies (ANA).

Most patients improve following withdrawal of

offending drug.
SLE

Hx and PE
Presence of ANA is a cardinal feature, but a (+)
ANA is not specific for SLE.

Treatment:
Goals are to control acute, severe
flares and to develop maintenance
strategies where symptoms are
suppressed to an acceptable level.
Choices depends on:
whether disease is life threatening or likely to
cause organ damage.
Choices depends on:
Whether manifestations are reversible.
and the best approach to prevent
complications of disease and treatment

Conservative Tx:

NSAIDS (e.g. ibuprofen 400-800 mg tid or qid,)

Antimalarials(hydroxychloroquinine 400
mg/day)
Tx for life- threatening SLE

Systemic glucocorticoids
Cytotoxic/ immunosupressive agents- added to
glucocorticoids to treat serious SLE.
Cyclophosphamide
Mycophenolate mofetil
Azathioprine
Anticoagulation- may be indicated in patients
with thrombotic complications.

Rheumatoid Arthritis
A chronic multisystem disease of unknown
etiology characterized by persistent
inflammatory synovitis, usually involving
peripheral joints in a symmetric fashion.

Although cartilaginous destruction, bony

erosions, and joint deformity are hallmarks, the
course of RA can be quite variable.
Clinical Manifestations:

women affected 3x more often than men

Frequent in the fourth and fifth decades.

Articular Manifestations:

Typically a symmetric polyarthritis of peripheral

joints with pain, tenderness and swelling of
affected joints.

Morning stiffness is common

PIP and MCP joints are frequently involved

Joint deformities may develop after persistent

inflammation.
Extra-Articular Manifestations:

Cutaneous- rheumatoid nodules, vasculitis

Pulmonary- nodules, interstitial disease

Ocular- keratoconjunctivitis sicca, episcleritis,

scleritis

Hematologic- anemia, Feltys

syndrome( splenomegaly and neutropenia)

Cardiac- pericarditis,myocarditis

Neurologic- myelopathies secondary to cervical

spine disease, vasculitis.
Evaluation:

Hx and PE with careful examination of all the

joints.

RF is present in > 66% of patients; its presence

correlates with severe disease, nodules, extraarticular features.

Antibodies to cyclic citrullinated protein(antiCCP) may be most useful in early RA.

Presence most common in patients with

aggressive disease with a tendency for
developing bone erosions.

ESR

Radiographs- juxtaarticular osteopenia, joint

space narrowing, marginal erosions. CXR
should be obtained.
Treatment:

Goals: lessen pain, reduce inflammation,

improve/maintain function, prevent long term
damage, control of systemic involvement.

Patient education

PT and OT

Aspirin or NSAIDS

Intraarticular glucocorticoids

Systemic glucocorticoids

Osteoarthritis

Disorder characterized by progressive joint

failure in which all structures of the joint have
undergone pathologic change.

Hyaline articular cartilage loss accompanied by

increasing thickness and sclerosis of the
subchondral bone plate.

Outgrowth of osteophytes at the joint margin,

stretching of the articular capsule, and
weakness of the muscles bridging the joint.

Most common type of arthritis.

Prevalence correlates strikingly with age.

More common in women.

Joint vulnerability and joint loading are the 2

major factors.

Other factors includes age, female, genetic

factors, joint trauma, previous damage,
malalignment, proprioceptive deficiencies and
obesity.

Earliest changes may begin in cartilage.( 2

major components are type 2 collagen which
provides tensile strength, and aggrecan, a
proteoglycan.

OA cartilage is characterized by gradual

depletion of aggrecan, unfurling of the collagen
matrix, and loss of type 2 collagen, which leads
to increased vulnerability.

Affects almost any joint but usually occurs in

weight bearing joints such as knee, hip, spine
and hands.( PIP, DIP, 1st carpometacarpal.
SYMPTOMS:

Use- related pain affecting one or a few

joints( rest and nocturnal pain less common).

Stiffness after rest or in morning may

occur(<30 mins).

Loss of joint mobility

Joint instability

Joint deformity

Joint crepitation (crackling)

Physical Examination

Chronic monoarthritis or asymmetric

oligo/polyarthritis.

Heberdens nodes(hand DIP)

Bouchards nodes (hand PIP)

Crepitance

Deformity

Restriction of motion

Objective neurologic abnormalities may be

seen with spine movements.
EVALUATION:

ESR usually normal but may be elevated in

patients who have synovitis.

RF, ANA studies negative.

Joint fluid is straw-colored with good viscosity.

Fluid WBC < 1000/microliter

Radiographs may be normal at first.

As disease progresses, may show joint space

narrowing, subchondral bone sclerosis,
subchondral cysts, and osteophytes.

Erosions are distinct as they occur

subchondrally along the central portion of the
joint surface.
TREATMENT:

Goal: alleviate pain and minimize loss of

physical function.

Patient education, weight reduction,

appropriate use of cane and other support,
isometric exercises to strengthen muscles
around the affected joints.

Bracing/orthotics to correct malalignment.

Acetaminophen, salicylates, NSAIDS, COX-2

inhibitors(selective and wont affect GI organ)
Tramadol
Intraarticular glucocorticoids

GOUT

Metabolic disease most often affecting middleaged to elderly women and postmenopausal
women.

Hyperuricemia is the hallmark. Overproduction

of uric acid.
CLINICAL MANIFESTATIONS:

Acute arthritis- most frequent early

manifestation of gout.

Initially affects one joint but may be

polyarticular in later episodes.

First metatarsophalangeal joint(podagra) is

often involved.

Acute gout frequently begins at night with

dramatic pain.

Attack will generally subside after 3 to 10 days.

Some patients may have a single attack.

Most will have recurrent episodes with intervals

of varying length with no symptoms between
attacks.

Acute gout may be precipitated by dietary

excess (beans, peanuts =daghan ug uric acid),
trauma, excessive ethanol ingestion, and
serious medical conditions such as MI, and
stroke.

Chronic Arthritis- a proportion may have

chronic non symmetric synovitis.

Can also present with periarticular

tophi(aggregates of MonoSodiumUric (MSU)
crystals sorrounded by a giant cell
inflammatory reaction) in chronic gout.

Extraarticular tophi- often occurs in olecranon

bursa, helix and antihelix of ears, ulnar surface
of arm and achilles tendon.

Tenosynovitis

Urate Nephropathy- can cause renal

insufficiency.

Uric acid nephrolithiasis (stone formation)responsible for 10% of renal stones in the U.S.
DIAGNOSIS:

Synovial Fluid Analysis- presence of MSU

crystals.

Serum Uric Acid-normal levels do not rule out

gout.

Urine Uric Acid- excretion of > 800mg/day on

regular diet in the absence of drugs suggests
overproduction.

Measurement of Erythrocyte Hypoxanthine

Guanine Phosphoribosyl Transferase (HGPRT)
and 5-phosphoribosyl-1-pyrophosphate (PRPP)
if overproduction is suspected.
Treatment:

Treatment of asymptomatic hyperuricemia is

not indicated.

Tx is given for symptomatic relief only since

attacks are self-limited and will resolve
spontaneously.

Analgesia

NSAIDS-DOC when not contraindicated.

Colchicine- generally effective within first 24

hours of attack.

Intraarticular glucocorticoids- septic arthritis

must be ruled out prior to injection.

Systemic Glucocorticoids
Uric Acid Lowering Agents- should not be given
during an acute attack.
Allopurinol-decrease uric acid synthesis by
inhibiting xanthine oxidase.

Uricosuric Drugs- probenicid, sulfinpyrazone.

Increase uric acid excretion by inhibiting its
tubular reabsorption.