Rheumatoid Arthritis and Gout

Muhamad Suffian bin Sentusa @ Md Daud2014430784

MUSCULOSKELETAL DISORDERS (PHT521)

Pn. Hjh. Rohani bt. Haron

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Table of Content

Content Slide no.

RHEUMATOID ARTHRITISIntroductionClassificationCausesPathophysiologyClinical features and AssessmentComplications

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GOUTIntroductionClassificationCausesPathophysiologyClinical features and AssessmentComplications

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References 292

Rheumatoid Arthritis

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Introduction•Rheumatoid arthritis (RA) is the most common persistent inflammatory arthritis affecting all ethnic groups throughout the world. (Davidson, 2010)(p. 1088)•The clinical course is prolonged and recurrent. Patients with RA have a greater mortality when compared with age-matched controls, mainly due to cardiovascular disease. This is most noticeable in those with severe disease, with expected 8-15 years reduce in lifespan. Around 40% of RA patients are registered disabled within 3 years, around 80% are somewhat to be severely disabled within 20 years and 25% will need a large joint replacement. (Davidson, 2010) (p. 1088)•Functional capacity diminishes most rapidly at the starting of disease and the functional status of patients within their first year of RA is usually based on long-term outcome. (Davidson, 2010) (p. 1088)•Rheumatoid arthritis is a chronic inflammatory disease featured by uncontrolled abundance of synovial tissue and a broad range of multisystem comorbidities. (Muller & Rakel, 2012) (p. 610)

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Classification

• It is crucial to diagnose and initiate treatment for RA as soon as possible to slow down the disease process and progression to major damage.• The 1987 RA classification criteria of the American College of

Rheumatology is the most widely used and recognized classification criteria for RA.• A patient shall be said to have RA if he/she has satisfied at least 4 of 7

of these criteria.• Criteria 1 to 4 must have been present for at least 6 weeks.

Weisman (2011) pp. 7-95

Weisman (2011) pp. 7-96

• 2010 American College of Rheumatology/European League Against Rheumatism Classification Criteria for RA are aimed at classification of newly presenting patients.• The target population is patients who have at least 1 joint with

definite clinical synovitis (swelling) and with the synovitis not better explained by another disease.• A score of ≥ 6/10 is needed for classification of patient as having

definite RA.

Weisman (2011) pp. 7-97

The 2010 American College of Rheumatology/European League Against Rheumatism Classification Criteria for RA Score

A. Joint involvement 1 large joint 2-10 large joints 1-3 small joints 4-10 small joints >10 joints (at least 1 small joint)

score

01235

B. Serology (at least 1 test result is needed for classification) Negative RF and negative ACPA Low-positive RF or low-positive ACPA High-positive RF or high-positive ACPA

023

C. Acute phase reactants (at least 1 test result is needed for classification) Normal CRP and abnormal ESR Abnormal CRP and abnormal ESR

01

D. Duration of symptoms < 6 weeks ≥ 6 weeks

01

Weisman (2011) pp. 7-98

Causes

• Actual cause is still unknown but not contagious.• Genetics• Can run in family but having it doesn’t greatly increase risk to the person’s

children.• Specific genetic marker; HLA-DR4 occurs in more than two thirds of men and

women who have RA.• People who have the marker not necessarily destined to have RA as one of

five people who do not have RA also have HLA-DR4.

Flynn & Johnson (2007) p. 429

• Infections • Some researchers think that exposure to some bacteria or viruses can cause

the abnormal immune response that cause RA among people who are genetically vulnerable.

• Environmental factors• Several studies found that heavy smokers and people heavily exposed to

cigarette smoke are prone to have rheumatoid arthritis than non-smokers.• Eating a diet rich in red meat and other high-protein foods may increase the

risk of RA.• Stress and psychological factors are also connected to RA.

Flynn & Johnson (2007) p. 4210

Pathophysiology

•The exact pathophysiologic flow is not yet defined.•RA is mostly caused by a pathologic immune response in a hereditarily susceptible person to an environmental upset, probably a viral or bacterial infection.•Epidemiologic reports show that genes encoding the class II major histocompatibility antigens are connected to clinical features of RA.•The HLA-DR4 and DR1 proteins appear self-antigens and foreign to T cells and presumed to play a direct part in RA.• Stress and psychological factors are also related to RA and to disease worsening. In a research, psychological factors and depression caused for at least 20% of disability in patients with RA, greater than the 14% accountable to articular signs and symptoms. In another research, helplessness had a direct effect on disease activity.

Muller & Rakel (2012) p. 61011

•Although it is believed that RA may be caused by an infectious agent in a genetically susceptible host, a specific pathogen has not been identified. Susceptibility is increased in childbirth and breastfeeding. Cigarette smoking also a strong risk factor for developing RA and causing greater severity.•Despite the initiating stimulus, RA is portrayed by lymphocytes, plasma cells and macrophages penetrate the synovial membrane with T cells play a main role by reacting with other cells in the synovium. •Activated T cells promote B cells to produce immunoglobulins including Rheumatoid Factor, and macrophages to produce pro-inflammatory cytokines. These reaction on endothelium, synovial fibroblasts, bone cells and chondrocytes promote swelling and clogging of the synovial membrane and damaging bone, cartilage and soft tissues. The pro-inflammatory cytokine TNF-α plays an significant part in this process by controlling other cytokines production.

Davidson (2010) pp. 1088-108912

•Release of immunoglobulins, including Rheumatoid Factor by B cells develop immune complexes within the joint and in extra-articular tissues, leading to vasculitis. Lymphoid follicles form in the synovial membrane. Inflammatory granulation tissue disperse under and over the articular cartilage that progressively worn and damaged. Later, fibrous or bony ankyloses may occur and muscles adjacent to inflamed joints atrophy and may be infiltrated with lymphocytes.•Rheumatoid nodules consist of a central area of fibrinoid material enclosed by proliferating mononuclear cells. Granulomatous lesions may follow in the pleura, lung, pericardium and sclera. Lymph nodes in RA are usually hyperplastic, showing many lymphoid follicles with large germinal centres and numerous plasma cells in the sinuses and medullary cords. Immunofluorescence confirms plasma cells in synovium and lymph nodes synthesize RF.

Davidson (2010) pp. 1088-108913

Clinical FeaturesClinical Features Assessment

Pain and stiffness•affecting the small joints of the hands, feet and wrists but large joint involvement, systemic symptoms and extra-articular features may also occur.

Visual Analog Scale for PainGoniometry for stiffness

Characteristic deformities •acquired through long-standing disease, including ‘swan neck’ deformity, the boutonnière or ‘button hole’ deformity, and a Z deformity of the thumb.

Observation

Posterior subluxation of the ulna at the distal radio-ulnar joint•contribute to rupture of the fourth and fifth extensor tendons. Triggering of fingers may occur because of nodules in the flexor tendon sheaths.

Radiography

Symmetrical swelling of the metacarpophalangeal (MCP) joints and proximal IP joints•actively inflamed if they are tender on pressure, and have stress pain on passive movement or effusion/soft tissue swelling.

Observation

Davidson (2010)14

Clinical Features Assessment

Calcaneovalgus (eversion) in the hindfoot •related with loss of the longitudinal arch (flat foot) due to tibialis posterior tendon’s rupture.

Posterior subluxation of the MTP joints in the foot•may cause ‘cock-up’ toe deformities. This causes pain on weight-bearing on the exposed MTP heads and development of secondary adventitious bursae and callosities.

Radiography

Popliteal (‘Baker’s’) cysts•occur in combination with knee synovitis, where synovial fluid link with the cyst but returning to the joint blocked by a valve-like mechanism.•Rupture often caused by knee flexion in the presence of a large effusion leads to calf pain and swelling.

Radiography

Davidson (2010)15

Complications

• Peripheral neuropathy – affect nerves of the feet and hand causing numbness, burning and tingling sensations.• Anaemic conditions – total red blood cell count decreases

considerably, body producing more white blood cell.• Elderly susceptible to infections as their immune system is weaker.• Scleritis – inflammation of the blood vessels in the eye resulting

corneal damage.• Various skin problems, periodontal diseases, gastrointestinal disorder,

heart ailments and lung diseases.• Osteoporosis is common for menopausal women.

Batty (2008) (p. 36 & 37). 16

Gout

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Introduction•Gout has been known since ancient times, with mentions by Egyptians as early as 2640 B.C. In the fifth century B.C., Hippocrates stated gout as ‘the un-walkable disease.’ Gout has also been called ‘the disease of kings’ because of the link with the intake of heavy foods and alcohol, common in the ruling class members. The name ‘gout’ is originated from Latin gutta [drop], referring to a drop of one of the four medieval humors once supposed to rule our health. (Hameed & Rakel, 2012)•Gout can be defined as the presence of monosodium urate monohydrate (MSU) crystals due to pathological reaction of the joint or periarticular tissues to the. MSU crystals deposit in peripheral connective tissues around and in synovial joints. (Davidson, 2010)•Gout prone to affect lower instead of upper limbs and specifically affecting the first MTP joint and small joints of feet and hands. There is gradual involvement of more proximal sites and the potential for cartilage and bone damage, with ‘secondary’ OA as the crystal deposits. MSU crystals need months or years to enlarge to a detectable size, indicating a long asymptomatic stage. (Davidson, 2010)

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ClassificationTo classify a case as gout it is necessary: Author’s comment on the selected criteria

To find uric acid crystals in synovial fluid or tissue (tophi)

Standard practice for gout diagnosis

Or the presence of two or more of the following:

History or observation of at least two attacks of painful limb swelling with remission within 1-2 weeks

These symptoms have been recognized in majority of patients as characteristic of a gout flare experience

History or observation of podagra Highly sensitive and specific location for gout flares

Presence of tophus Highly specific finding but it is a late occurrence in majority of the patients.

History or observation of a good response to colchicine (major reduction in objective signs of inflammation within 24 hours of onset of the therapy)

Major response to colchicine is not present in majority of gout patients according to most recent randomized trial.

New York Criteria for the Classification of Gout (1968)

Terkeltaub (2011), p. 10119

Causes

• Exact cause of primary gout is unknown.• May be caused by genetic defect in purine breakdown causing

overproduction of uric acid, retention of uric acid or both.• Some patients are intrinsic ‘over-producers’ of uric acid through no

identifiable cause or if there is a family history of early-onset gout.

Unknown (2011) p. 379

• In secondary gout, it results from hyperuricaemia due to renal impairment or chronic diuretic use.• Diuretic can cause decrease urate excretion (ionic form of uric acid).• High alcohol intake (especially beer which contains guanosine) • Guanosine is one of purine nucleotide. • More alcohol intake means more uric acid.

• Diets relatively high in red meat or fructose or relatively low in vitamin C or coffee.

21Unknown (2011) p. 379

Pathophysiology •When uric acid is supersaturated in blood and other body fluids, it crystallizes and forms a deposit of urate salts that accumulate in connective tissue throughout the body; these deposits are called tophi. The presence of the crystals triggers an acute inflammatory response when neutrophils begin to ingest the crystals. Tissue damage begins when the neutrophils release their lysosomes. Lysosomes not only damage the tissue but also spread the inflammation.•In asymptomatic gout, the serum urate level increases but the urate doesn’t crystallize or produce symptoms. As progress, it may cause hypertension or urate kidney stones.•The first acute attack strikes suddenly and peaks quickly. Although it generally involves only one or a few joints, this initial attack is extremely painful. Affected joints appear hot, tender, inflamed, dusky red or cyanotic.

22Unknown (2011) pp. 379-380

•The MTP joint of the great toe usually becomes inflamed first ( podagra), then the instep, ankle, heel, knee, or wrist joints. Sometimes a low-grade fever is present. Mild acute attacks typically subside quickly but tend to recur at irregular intervals. Severe attacks may persist for days or weeks.•Most patients have a second attack within 6 months to 2 years but some attacks common in those who are untreated, tend to be longer and more severe than initial attacks. Such attacks are also polyarticular, invariably affecting joints in the feet and legs, and sometimes accompanied by fever. A migratory attack sequentially strikes various joints and the Achilles tendon and is associated with either subdeltoid or olecranon bursitis.•Eventually, chronic polyarticular gout sets in. this final, unremitting stage of the disease is marked by persistent painful polyarthritis with large tophi in cartilage, synovial membranes, tendons and soft tissue. Tophi form in fingers, hands, knees, feet, ulnar sides of the forearms, helices of the ears, Achilles tendons and rarely, in internal organs such as the kidneys and myocardium. The skin over the tophus may ulcerate and release a chalky, white exudate that’s composed primarily of uric acid crystals.

23Unknown (2011) pp. 379-380

Clinical Features

Clinical features Assessment

Joint pain•Usually described as the ‘worst pain ever’

Visual Analog Scale for Pain

Extremely rapid onset•maximum severity in just 2–6 hours, always waking the patient in the early morning

Ask the patient

Extreme tenderness•unable to wear a sock or to let bedding rest on the joint

Swelling•overlying red, shiny skin

Observation

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Acute Gout

Davidson (2010) pp. 1098

Clinical features Assessment

Synovitis, periarticular swelling and erythema Observation

May be accompanied by fever, malaise and confusion if a large joint such as the knee is involved.

Pruritus and peeling of the skin as the attack reduces

Observation

25Davidson (2010) pp. 1098

Chronic and recurrent goutClinical features Assessment

Joint damage•Caused by continued urate salt deposition

Chronic pain•interval between the first attack and the development of chronic symptoms is variable but averages around 10 year

VAS for Pain

There may be severe deformity especially hands and feet

Observation

Marked functional impairment of hands and feet•Restricted movement

Goniometry

26Davidson (2010) pp. 1099

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Clinical features Assessment

Asymmetry tophi•The tophi produced on the joint is not symmetry each side.

Radiograph

Irregular firm nodules (‘tophi’) around extensor surfaces of fingers, hands, forearm, elbows, Achilles tendons and occasionally the helix of the ear.•Due to large MSU crystal deposition usually in chronic renal failure patient.

Observation

Davidson (2010) pp. 1099

Complications

• Lasting erosions, deformity and disability because of chronic inflammation and tophi that cause secondary joint degeneration.• Hypertension and albuminuria (in some patient).• Involvement of the kidney with tubular damage from deposition of

urate crystal causing poorer excretion of uric acid and chronic renal dysfunction.

Unknown (2011) pp. 38028

References• Batty, P. (2008). Living with Rheumatoid Arthritis (p. 36 & 37). EFortune US.

• Davidson, S. (2010). Inflammatory Joint Disease. In Davidson's Principles and Practice of Medicine (21st ed., pp. 1088-1091,1097-1100). Elsevier Inc.

• Flynn, J., & Johnson, T. (2007). Rheumatoid Arthritis. In Arthritis (p. 42). Baltimore, Maryland: Johns Hopkins Health.

• Hameed, F. & Rakel, D. (2012). Gout. In Integrative Medicine (p. 610). Philadelphia, PA: Elsevier.

• Muller, D. & Rakel, D. (2012). Rheumatoid Arthritis. In Integrative Medicine (p. 456). Philadelphia, PA: Elsevier.

• Professional guide to pathophysiology (3rd ed., pp. 379-380). (2011). Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins.

• Terkeltaub, R. (2012). Diagnosis of Gout. In Gout and other crystal arthropathies (p. 101). Philadelphia, PA: Saunders/Elsevier.

• Weisman, M. (2011). Definition and Classification. In Rheumatoid Arthritis (pp. 7-9). New York: Oxford University Press.

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