Medicine 5th year, all lectures/rheumatology (Dr. Rauf)

RheumatologyRheumatology
Rheumatology is concerned with diseases ofRheumatology is concerned with diseases of
joints & C.T., they are diseases of musculoskeletaljoints & C.T., they are diseases of musculoskeletal
system.system.
Rheumatological conditions are characterized by ,Rheumatological conditions are characterized by ,
chronic pain, stiffness &progressive impairment ofchronic pain, stiffness &progressive impairment of
joints & soft tisssue.joints & soft tisssue.
Economically they are costy , the cost comes fromEconomically they are costy , the cost comes from
the direct spent of treatment ( direct cost) &the direct spent of treatment ( direct cost) &
indirect cost from the lost of productivity.( theseindirect cost from the lost of productivity.( these
costs are millions of dollars).costs are millions of dollars).

Rheumatolgical conditions are one of the majorRheumatolgical conditions are one of the major
causes of disabilities in community.causes of disabilities in community.
They may lead to various types of disabilities whichThey may lead to various types of disabilities which
could be ;could be ;
1-Physical diability1-Physical diability ( walking, bending,lifting &( walking, bending,lifting &
grasping).grasping).
2-Social disability2-Social disability ( refers to higher tasks ,( refers to higher tasks ,
i.e.eating, dressing, shopping& interacting withi.e.eating, dressing, shopping& interacting with
other people.)other people.)
Arthritis first causes of physical dysfunction whichArthritis first causes of physical dysfunction which
lead to social dysfunction.lead to social dysfunction.

Social dysfunction includes :Social dysfunction includes :
1-1-Basic personal care tasks ( ADL) such as eating ,Basic personal care tasks ( ADL) such as eating ,
grooming& toileting.grooming& toileting.
2-2-Instrumental activities of daily living(IADL)Instrumental activities of daily living(IADL)
(house task) like shopping and paying bills.(house task) like shopping and paying bills.

JOINTS.JOINTS.
Joint is articulation between two or more bones.Joint is articulation between two or more bones.
The activities of human body depends on effectiveThe activities of human body depends on effective
interaction between normal joints & neuromuscularinteraction between normal joints & neuromuscular
units that drive them.units that drive them.
Types of joints are:Types of joints are:
1.1. Synarthrosis ( skull joints)Synarthrosis ( skull joints)
2.2. Amphiarthrosis( Cartilaginous joints) haveAmphiarthrosis( Cartilaginous joints) have
modest motion ( Intervertebral disc joints).modest motion ( Intervertebral disc joints).
3.3. Diarthrosis are mobile joints have synovialDiarthrosis are mobile joints have synovial
membrane (synovial joints ).membrane (synovial joints ).

Anatomy of synovial joints.Anatomy of synovial joints.
Diarthroidal joint consist of :Diarthroidal joint consist of :
1.1. Opposing bony surfaces.Opposing bony surfaces.
2.2. Hyaline cartilage covering the articulating surfaces ofHyaline cartilage covering the articulating surfaces of
bones.It is firmly attached to the underlying bone.bones.It is firmly attached to the underlying bone.
It is aneural & avascular. It gets the nourishmentIt is aneural & avascular. It gets the nourishment
from synovial fluid , s. membrane &underlying bone.from synovial fluid , s. membrane &underlying bone.
The cartilage is shock absorber.The cartilage is shock absorber.
3.3. Capsule which is surrounding the articular tissue.Capsule which is surrounding the articular tissue.

4.4. Synovial membrane which lines the capsule.Synovial membrane which lines the capsule.
Has A cells are macrophage like cells haveHas A cells are macrophage like cells have
phagocytic function & B cells are fibroblastphagocytic function & B cells are fibroblast
like cells ( produce hyaluronate part oflike cells ( produce hyaluronate part of
synovialsynovial
fluid.fluid.
5.5.Joint cavity.Joint cavity.
6.6. Synovial fluid. Is viscous , pale yellow & clearSynovial fluid. Is viscous , pale yellow & clear
fluid , present in small amount ranging fromfluid , present in small amount ranging from
( 0.1 _ 4). Hyaluronic acid making the fluid( 0.1 _ 4). Hyaluronic acid making the fluid
viscous.The fluid lubricates the joint.viscous.The fluid lubricates the joint.

Rheumtology ;Rheumtology ; is concerned with the diseases ofis concerned with the diseases of
joints & C.Ts which could be damaged by avarietyjoints & C.Ts which could be damaged by avariety
of pathological processes ( infectionof pathological processes ( infection
,inflammation,inflammation
, degeneration, metabolic disturbances &systemic, degeneration, metabolic disturbances &systemic
diseases like leukaemia or Haemochromatosis.diseases like leukaemia or Haemochromatosis.

Rheumatological Terminology.Rheumatological Terminology.
Arthritis:Arthritis: is inflammation of the joint.is inflammation of the joint.
Polyarthritis :Polyarthritis : is inflammation of five or moreis inflammation of five or more
joints simultaneously.joints simultaneously.
Oligoarthritis ( Pauciarticular) :Oligoarthritis ( Pauciarticular) : 2_ 4 joint are2_ 4 joint are
involved.involved.
Monoarthritis :Monoarthritis : is inflammation of one joint.is inflammation of one joint.
Arthralgia :Arthralgia : is a joint pain without swelling .is a joint pain without swelling .

Inflammation of joint is suggested by :Inflammation of joint is suggested by :
Pain , Swelling, Warmth & reddening of overlyingPain , Swelling, Warmth & reddening of overlying
skin.skin.
Joint stiffness which occur after a period ofJoint stiffness which occur after a period of
immobility & lasting for over a period ( hour) isimmobility & lasting for over a period ( hour) is
more reliable indication of inflammation.more reliable indication of inflammation.
Reduction of joint motion & loss of function mayReduction of joint motion & loss of function may
occur in noninflammatory condition also.occur in noninflammatory condition also.

ClassificationClassification
Inflammatory arthritis.Inflammatory arthritis.
1.1. R.A.R.A.
2.2. Seronegative arthropathies.Seronegative arthropathies.
3.3.C.T diseases : SLE.C.T diseases : SLE.
Scleoderma.Scleoderma.
Dermatomyositis.Dermatomyositis.
4.4.Crystal induced arthropathies.Crystal induced arthropathies.
5.5.Degenerative joint disease : primary or secondary.Degenerative joint disease : primary or secondary.

6.6. Arthritis associated with infection :Arthritis associated with infection :
( septic &nonseptic arthritis).( septic &nonseptic arthritis).
7.7. Arthritis associated with systemic diseasesArthritis associated with systemic diseases
(bacterial endocarditis, acromegaly, thyroid(bacterial endocarditis, acromegaly, thyroid
diseases,respiratory diseases & miscellaneous-diseases,respiratory diseases & miscellaneous-
sarcoidosis,amyloidosis etc.sarcoidosis,amyloidosis etc.
8.8. Nonarticular rheumatism& localized painNonarticular rheumatism& localized pain
(tenosynovitis, bursitis,fibrositis&enthesopathies)(tenosynovitis, bursitis,fibrositis&enthesopathies)

CLINICAL FEATURESCLINICAL FEATURES
Features help in the diagnosis of arthritis in generalFeatures help in the diagnosis of arthritis in general
are :are :
Age:Age: as in OA.as in OA.
Gender:Gender: RA & SLE are more common in females.RA & SLE are more common in females.
Race:Race: As arthritis associated with sickle cellAs arthritis associated with sickle cell
anemia.anemia.
Occupation:Occupation: As in soft tissue rheumatism.As in soft tissue rheumatism.

Joint pain:Joint pain: the following points are of some valuethe following points are of some value
to in the diagnosis of arthritic problemsto in the diagnosis of arthritic problems
regardingregarding
pain :pain :
Duration of painDuration of pain ( in Gout is acute while in RA is( in Gout is acute while in RA is
usually chronic).usually chronic).
Onset:Onset: ( abrupt in gout).( abrupt in gout).
Precipitating factors:Precipitating factors: as trauma, use of diureticsas trauma, use of diuretics
etc.etc.

CharacterisiticsCharacterisitics
 Site of pain : This usually indicates the site ofSite of pain : This usually indicates the site of
the pathology.the pathology.
 Radiation.Radiation.
 Severety: i.e. Gout.Severety: i.e. Gout.
 Aggravating & relieving factors.Aggravating & relieving factors.
 Diurnal variation.( i.e.Inflammation).Diurnal variation.( i.e.Inflammation).
Episodic arthritisEpisodic arthritis
Morning Stiffness.Morning Stiffness. Duration is important.Duration is important.
Pattern of joint involvement.Pattern of joint involvement.
Reccurent attack, small joints involvement.Reccurent attack, small joints involvement.
Disability.Disability. ( depends on joints affected).( depends on joints affected).

Objective singes of arthritis.Objective singes of arthritis.
Swelling , Tenderness, Limitation of jointSwelling , Tenderness, Limitation of joint
movement , deformity, Crepitas & Heat &movement , deformity, Crepitas & Heat &
redness.redness.
Joint pathology is indicated by pain & one or ofJoint pathology is indicated by pain & one or of
other signes.other signes.
Five cardinal singes of inflammation are :Five cardinal singes of inflammation are : swelling,swelling,
warmth, erythema, tenderness & loss of function.warmth, erythema, tenderness & loss of function.
Joint examination:Joint examination:
Includes three stages.( Look at it , feel it & move it)Includes three stages.( Look at it , feel it & move it)

Lab. Tests:Lab. Tests:
1.ESR1.ESR
2.CRP(c-reactive protein)2.CRP(c-reactive protein)
3.Hb3.Hb
4.WBCs count4.WBCs count

Rheumatoid factors.Rheumatoid factors. Are autoantibodiesAre autoantibodies
directed against antigenic determinants on the FCdirected against antigenic determinants on the FC
fragment of immunoglbuline G. RF may be of anyfragment of immunoglbuline G. RF may be of any
isotype IgG, IgM, IgA or IgE.IgM is the oneisotype IgG, IgM, IgA or IgE.IgM is the one
routinely measured by clinical laboratories.routinely measured by clinical laboratories.
RF is detected by agglutination of either latexRF is detected by agglutination of either latex
particles or sheep red cells.particles or sheep red cells. Also by ELISA &Also by ELISA &
Nephelometry.Nephelometry.
Anti-CCP( anticyclic citriullinated peptide antibodies) areAnti-CCP( anticyclic citriullinated peptide antibodies) are
autoantibodies directed against the amino acids , it’s believed thatautoantibodies directed against the amino acids , it’s believed that
have a role in the pathogenisis of RA.have a role in the pathogenisis of RA.
Antinuclear antibodies( ANA).Antinuclear antibodies( ANA). Are antibodiesAre antibodies
which react to constituents of nucleous ( SLE ,which react to constituents of nucleous ( SLE ,
Scleroderma, Juvenile RA. Etc.).Scleroderma, Juvenile RA. Etc.).
Serum uric acid ; ( GOUT).Serum uric acid ; ( GOUT).

Imagings :Imagings :
Plain x-ray is important in OA, RA & otherPlain x-ray is important in OA, RA & other
rheumatological conditions. i.e ( osteophyte ,rheumatological conditions. i.e ( osteophyte ,
erosion….).erosion….).
C.C.T scan & MRI are now more valuable than x-rayT scan & MRI are now more valuable than x-ray
in diagnosis.in diagnosis.

Synovial fluid anlysis:Synovial fluid anlysis:
Is helpful in distinguishing between inflammatoryIs helpful in distinguishing between inflammatory
& noninflammatory arthritis. It is diagnostic in& noninflammatory arthritis. It is diagnostic in
crystal induced arthropathies ( gout) & septiccrystal induced arthropathies ( gout) & septic
arthritis.arthritis.
SynovialSynovial biopsy:biopsy:
done through needle biopsy or by arthroscopydone through needle biopsy or by arthroscopy
(which by itself is a valuable investigation).(which by itself is a valuable investigation).

Ultrasound of joint & soft tissues.Ultrasound of joint & soft tissues.
Radioisotope bone scan:Radioisotope bone scan: ( tumors, infection,( tumors, infection,
trauma, lead to increased uptake.).trauma, lead to increased uptake.).
Histocompatability antigens:Histocompatability antigens: i.ei.e HLAB27 in ASHLAB27 in AS
95% , Reiter’s disease 60% positive.95% , Reiter’s disease 60% positive.
Some other investigations are helpfulSome other investigations are helpful::
serum alkaline phophataseserum alkaline phophatase
ASOASO
low serum complements ( in SLE).low serum complements ( in SLE).

Osteoarthritis.Osteoarthritis.
OA.Is a disease of diarthroidal joints , is aOA.Is a disease of diarthroidal joints , is a
commonest musculoskeletal disease.commonest musculoskeletal disease.
Charecterised byCharecterised by
1.1. pain & limitation of function,pain & limitation of function,
2.2. osteophyte & joint space narrowing.osteophyte & joint space narrowing.
3.3. Alteration in cartilage integrity.Alteration in cartilage integrity.
4.4. NO systemic manifestations.NO systemic manifestations.
The disease occurs through the world &The disease occurs through the world &
through the history, it is more common in females.through the history, it is more common in females.

Pathogenesis & pathologyPathogenesis & pathology..
It is a disease of articular cartilage.It is a disease of articular cartilage.
Chondrocytes are maintaining homeostasis ofChondrocytes are maintaining homeostasis of
cartilage , it synthesize collagens, proteoglycans &cartilage , it synthesize collagens, proteoglycans &
proteinases.proteinases.
OA results from failure of chondrocytes toOA results from failure of chondrocytes to
synthesize a good quality of matrix in terms ofsynthesize a good quality of matrix in terms of
elasticity & resistance & to maintain the balanceelasticity & resistance & to maintain the balance
between synthesis & degredation.between synthesis & degredation.
The degeneration process might be initiated byThe degeneration process might be initiated by
some stimuli ( Mechanical insult or Biochemicalsome stimuli ( Mechanical insult or Biochemical
abnormalities of cartilage).abnormalities of cartilage).

The chodrocyte is believed to start releasingThe chodrocyte is believed to start releasing
enzymes which degrade collagen & proteoglycan,enzymes which degrade collagen & proteoglycan,
breaks in the cartilage allow the uptake of water,breaks in the cartilage allow the uptake of water,
cartilage swells & splits leads to breaking of thecartilage swells & splits leads to breaking of the
cartilage( fibrillation of the surface) , clefts downcartilage( fibrillation of the surface) , clefts down
toward the bone surface, gradual lyses of cartilagetoward the bone surface, gradual lyses of cartilage
by synovial enzymes & inflammation of theby synovial enzymes & inflammation of the
synovial membrane ( might be effusion).synovial membrane ( might be effusion).

The underneath bone become smooth & hardThe underneath bone become smooth & hard
called ( eburnation) & osteophytes form fromcalled ( eburnation) & osteophytes form from
boney edges & subchondral bone cyst mightboney edges & subchondral bone cyst might
form.form.
Joint insability may develop as a result ofJoint insability may develop as a result of
capsulare laxity , collapse of subchondral bonecapsulare laxity , collapse of subchondral bone
cyst & muscular atrophy.cyst & muscular atrophy.

CLASSIFICATION OF OA. SCLASSIFICATION OF OA. S
A. Primary OA.A. Primary OA.
1.1. Localised ( Heberden s & Bouchard s nodes)Localised ( Heberden s & Bouchard s nodes)
2.2.Primary generlised OA.( involvement of 3 orPrimary generlised OA.( involvement of 3 or
mor joints or joint groups).mor joints or joint groups).

B. Secondary OA.B. Secondary OA.
Any malalignment , damage or alteration to theAny malalignment , damage or alteration to the
constituents of the joint ( the bone, cartilage,constituents of the joint ( the bone, cartilage,
capsule, ligamemts or synovium may result incapsule, ligamemts or synovium may result in
accelerated wear& the development of OA.accelerated wear& the development of OA.
1.1. Trauma.( Intraarticular fracture, maalignmentTrauma.( Intraarticular fracture, maalignment
ofof
ratcture, unequal leg length, occupation ).ratcture, unequal leg length, occupation ).
2.2. Genetic, congenital & developmentalGenetic, congenital & developmental
abnormalities: Hypermobility, DDH, Perth’sabnormalities: Hypermobility, DDH, Perth’s
disease etc.disease etc.

3.3. Post inflammatory ( RA, Septic arthritis etc).Post inflammatory ( RA, Septic arthritis etc).
4.4. Haemorrhage to the joint( Haemophilia).Haemorrhage to the joint( Haemophilia).
5.5. Metabolic & endocrine diseases.Metabolic & endocrine diseases.
6.6. Bone disorder( Paget s disease)Bone disorder( Paget s disease)
7.7. Neuropathic joints.Neuropathic joints.

Risk factors for OA are:Risk factors for OA are:
 Obesity,Obesity,
 Heridity( in DIP joints),Heridity( in DIP joints),
 Age,Age,
 Previous joint disease ( trauma),Previous joint disease ( trauma),
 Abnormal joint mechanics( varus or valgus) ,Abnormal joint mechanics( varus or valgus) ,
 Smoking( in disc disease).Smoking( in disc disease).

AetiologyAetiology
OA is probably is multifactorial .OA is probably is multifactorial .
1.1. Age & gender. OA is more in aged & females.Age & gender. OA is more in aged & females.
2.2. Trauma & obesity.Trauma & obesity.
3.3. Hormonal & metabolic causes.Hormonal & metabolic causes.
4.4. Genetic factor.Genetic factor.
5.5. Diatery causes.Diatery causes.

Clinical Features.Clinical Features.
Commonly affected joints are spine , knees, DIPs,Commonly affected joints are spine , knees, DIPs,
PIPs, thumb joint, & first MTP jointsPIPs, thumb joint, & first MTP joints
SymptpmsSymptpms
Pain.Pain.
Is deep dull aching pain, worse by use ( in evening) mayIs deep dull aching pain, worse by use ( in evening) may
be present at rest. Trauma precipitate it , related tobe present at rest. Trauma precipitate it , related to
weather ( more in cold & damp weather), it may radiate toweather ( more in cold & damp weather), it may radiate to
the surrounding structures.It may be persistent interferingthe surrounding structures.It may be persistent interfering
with normal function & sleep.with normal function & sleep.
Pain arises from structures possessing nerve endings &Pain arises from structures possessing nerve endings &
may result from microfructures in subchondral bone.may result from microfructures in subchondral bone.

Stiffness.Stiffness.
It is less sever than in inflammatory arthritis &It is less sever than in inflammatory arthritis &
lasts for a shorter period ( few minutes).lasts for a shorter period ( few minutes).
Disability.Disability.
It depends on a number & severity of jointIt depends on a number & severity of joint
affection.affection.

Signs of OASigns of OA
1.1. Swelling. May be due to soft tissue, fluid orSwelling. May be due to soft tissue, fluid or
boney overgrowth.boney overgrowth.
Heberdens & Bouchards nodes. Are bneyHeberdens & Bouchards nodes. Are bney
articular nodes. ( H.N are seen on DIPs & B.Narticular nodes. ( H.N are seen on DIPs & B.N
on PIPs).on PIPs).
2.2. Crepius.Crepius.
3.3. Signs of inflammation.Signs of inflammation.
4.4. Limitation of joint movement.Limitation of joint movement.
5.5. Joint deformity.( valgus, varus , flexionJoint deformity.( valgus, varus , flexion
deformities or joint instability).deformities or joint instability).
6.6. Loss of function.Loss of function.

Investigations.Investigations.
There are no diagnostic makers in OA.There are no diagnostic makers in OA.
X- Ray changes.X- Ray changes.
1.1. Narrowing of the joint spaceNarrowing of the joint space
2.2. Oteophyte.Oteophyte.
3.3. Sclerosis of subchondral bone ( eburnation).Sclerosis of subchondral bone ( eburnation).
4.4. Subchondral bone cyst.Subchondral bone cyst.
5.5.Deformity resulting from sublaxation.Deformity resulting from sublaxation.
6.6.Presence of loose bodies.Presence of loose bodies.
7.7.Irregularity of bone surfaces.Irregularity of bone surfaces.
MRI is superior to X-Ray ( showing cartilage changesMRI is superior to X-Ray ( showing cartilage changes).).

MANAGEMENTMANAGEMENT
Aims are.Aims are.
1.1. Relieving pain.Relieving pain.
2.2. Maintaining & improving joint function.Maintaining & improving joint function.
3.3. Preventing or minimizing disability improvingPreventing or minimizing disability improving
functioning.functioning.

General measures.General measures.
1.1. Education of the patient.Education of the patient.
2.2. Maintain & improve joint function.Maintain & improve joint function.
3.3. Short lower limb should be correted.Short lower limb should be correted.
4.4. Reduce weight .Reduce weight .
5.5. Avoid trauma.Avoid trauma.
6.6. Use aid .Use aid .
7.7. Change jobe.Change jobe.

Phamcological therapy.Phamcological therapy.
1.1. Simple analgesia( paracetamol).Simple analgesia( paracetamol).
2.2. NSAIDs.NSAIDs.
3.3. Intraarticular injections( steroid , Hyaluronic acid).Intraarticular injections( steroid , Hyaluronic acid).
4.4. New agents ( might reduce cartilage degredation &New agents ( might reduce cartilage degredation &
stimulate cartilage synthesis)( Glucosamininglycan &stimulate cartilage synthesis)( Glucosamininglycan &
chondroitoin ).chondroitoin ).
Physiotherapy.Physiotherapy.
To maintain joint mobility &function & improve muscularTo maintain joint mobility &function & improve muscular
condition.condition.
Surgery.Surgery.
( i.e joint replacement).( i.e joint replacement).

Rheumatoid Arthritis.Rheumatoid Arthritis.
Is a chronic systemic inflammatory disease ofIs a chronic systemic inflammatory disease of
unknown aetiology characterized byunknown aetiology characterized by
symmetrical arthritis of hands , feet & othersymmetrical arthritis of hands , feet & other
joints ( PIP & MCPs) with bone erosion.joints ( PIP & MCPs) with bone erosion.
RA is a commonest inflammatory arthritis.RA is a commonest inflammatory arthritis.
RA is characterized by:RA is characterized by:
1.1. A symmetrical inflammatory polyarthritis.A symmetrical inflammatory polyarthritis.
2.2. It has extraarticular features.It has extraarticular features.
3.3. Progressive joint damage causingt severProgressive joint damage causingt sever
disability in young people.disability in young people.

Epidemiology.Epidemiology.
RA is a world wide disease affects all racial &RA is a world wide disease affects all racial &
ethinic groups.It affects 1—3% of population ,ethinic groups.It affects 1—3% of population ,
female/ male is 3/1.female/ male is 3/1.
Age range is 10 – 70y. ( starts 30& 40ys.).Age range is 10 – 70y. ( starts 30& 40ys.).
5—10% having family history & 70% have5—10% having family history & 70% have
HLADR4.sHLADR4.s

Aetiology & Pathogenesis.Aetiology & Pathogenesis.
The cause of RA is unknown. Several factors mayThe cause of RA is unknown. Several factors may
possibly operate to produce the disease ( i.e.possibly operate to produce the disease ( i.e.
Genetic, environment..). RA is said to be anGenetic, environment..). RA is said to be an
autoimmune disease.( there are manyautoimmune disease.( there are many
immunological disturbances in RA. Asimmunological disturbances in RA. As
autoantibodies).( Cytochins , growth factors ,autoantibodies).( Cytochins , growth factors ,
tumor necrosis factors& metalloproteases havetumor necrosis factors& metalloproteases have
role in the production of the disease.).role in the production of the disease.).

Pathology.Pathology.
RA is a disease of synovial membrane.RA is a disease of synovial membrane.
There is Inflammation & proliferation.( synovitis occurThere is Inflammation & proliferation.( synovitis occur
with chronic inflammatory cells infiltration, lymphocyte,with chronic inflammatory cells infiltration, lymphocyte,
plasma cells & macrophages followedby gaintplasma cells & macrophages followedby gaint
cellsinfiltration, fibrinoid degeneration& hyperplasia ofcellsinfiltration, fibrinoid degeneration& hyperplasia of
lining cells followed by granulation tissue ( Pannus)lining cells followed by granulation tissue ( Pannus)
formation which is a tumor like mass. This leads toformation which is a tumor like mass. This leads to
detruction of the cartilage & bone & might be effusion.detruction of the cartilage & bone & might be effusion.
Synovitis occurs in tendon sheath & bursae. NodulesSynovitis occurs in tendon sheath & bursae. Nodules
might occur over pressure areas ( more on extensormight occur over pressure areas ( more on extensor
surfaces).surfaces).
Vasculitis( panarteritis) may occur.Vasculitis( panarteritis) may occur.
Chest could be involved.Chest could be involved.
Eyes might be affected.Eyes might be affected.

The onset is variable ( 70% insidious 15- 20% isThe onset is variable ( 70% insidious 15- 20% is
subacute & 5—10% acute while few havingsubacute & 5—10% acute while few having
episodic symptoms that progress to persistantepisodic symptoms that progress to persistant
diseases ).diseases ).
Commonly affected joints are MCPs, PIPs, wrists,Commonly affected joints are MCPs, PIPs, wrists,
MTPs & larger joints.MTPs & larger joints.
RA might starts with few joints then progress&RA might starts with few joints then progress&
become symmetric.become symmetric.

Thoracolumbare , sacroiliac & DIP joints are veryThoracolumbare , sacroiliac & DIP joints are very
rarely involved.rarely involved.
RA is generally symmetrical, destructive, disablingRA is generally symmetrical, destructive, disabling
& deforming polyarthritis , affecting small && deforming polyarthritis , affecting small &
large joints.large joints.
It has systemic manifestations, extraaricularIt has systemic manifestations, extraaricular
features& circulating antiglobulin antibodiesfeatures& circulating antiglobulin antibodies
(RA factor).(RA factor).

Symptoms.Symptoms.
1.1. Joint painJoint pain.( More in the morning & might.( More in the morning & might
disturb the sleep).disturb the sleep).
2.2. Morning stiffness.Morning stiffness. Is a prominent feature ,Is a prominent feature ,
present after aperoid of rest often lasts for severalpresent after aperoid of rest often lasts for several
hours.hours.
3.3. General symptpms.General symptpms. Malaise, fever,loss of weight &Malaise, fever,loss of weight &
strength & diffuse muscle wasting .strength & diffuse muscle wasting .
4.4. Disability.Disability. This depends on joints affected &This depends on joints affected &
destructions occurred.destructions occurred.
5.5. Non articular symptoms:eNon articular symptoms:e .g CTS..g CTS.

Signs.Signs.
 Swelling,Swelling,
 Warmth,Warmth,
 Limitation of movements,Limitation of movements,
 Deformities &Deformities &
 Nodules.Nodules.

Pettern of joint involvement.Pettern of joint involvement.
RA is usually starts from small joints of hands &RA is usually starts from small joints of hands &
feet but in most patients eventually many joints arefeet but in most patients eventually many joints are
involved ( wrists, knees, ankls , shoulders etc…).involved ( wrists, knees, ankls , shoulders etc…).

Hands & feet.Hands & feet.
MCPs &PIPs are early involved ( spindle shapeMCPs &PIPs are early involved ( spindle shape
swelling of PIPs). , Swelling of wrists.swelling of PIPs). , Swelling of wrists.
Progression of the disease will lead wasting &Progression of the disease will lead wasting &
atrophy of small muscles , weakening of capsuleatrophy of small muscles , weakening of capsule
& other supportive tissue & joint destruction result& other supportive tissue & joint destruction result
in limitation of joint motion , instability,in limitation of joint motion , instability,
sublaxation & deformities.sublaxation & deformities.

Hand deformities.Hand deformities.
Radial deviation at wrist.Radial deviation at wrist.
Ulnar deviation at MCP joints.Ulnar deviation at MCP joints.
Swan neck deformity ( hperextension at PIPs).Swan neck deformity ( hperextension at PIPs).
Boutonnier deformity( flexion at PIPS)Boutonnier deformity( flexion at PIPS)
Feet deformities are more or less are like thoseFeet deformities are more or less are like those
occur in hands.occur in hands.

The kneesThe knees..
1.1.Synovial effusionSynovial effusion
2.2.Deformities( valgus., varus &/ or flexion ).Deformities( valgus., varus &/ or flexion ).
3.3.Bakers cyst in popliteal fossa which mayBakers cyst in popliteal fossa which may
repture.( sudden onset of pain & swelling in calfrepture.( sudden onset of pain & swelling in calf
and ankle) diagnosed by US. & arthrogram.and ankle) diagnosed by US. & arthrogram.

PresentationsPresentations..
RA is commonly affecting small joints of hands & feet.RA is commonly affecting small joints of hands & feet.
It could be presented as acute polyathritis ( 15% ).It could be presented as acute polyathritis ( 15% ).
Involvement of large joints.Involvement of large joints.
Monoarticular is not uncommon.Monoarticular is not uncommon.
Palindromic( episodic).Palindromic( episodic).
Soft tissue involvement.Soft tissue involvement.
Prodromal systemic symptoms.Prodromal systemic symptoms.
With the progression of the disease get( destructiveWith the progression of the disease get( destructive
changes, deformities, symptoms of mechanical effects aschanges, deformities, symptoms of mechanical effects as
pressure on the nerves( CTS) ).pressure on the nerves( CTS) ).

Criteria for the diagnosis of RA.Criteria for the diagnosis of RA.
1.1. Morning stiffness for> one hour.Morning stiffness for> one hour.
2.2. Swelling of 3 or more joints( arthritis).Swelling of 3 or more joints( arthritis).
3.3. Swelling of hand joints ( PIPs , MCPs & wrist ).Swelling of hand joints ( PIPs , MCPs & wrist ).
4.4. Symmetrical polyarthritis.Symmetrical polyarthritis.
5.5. Subcutaneous nodules.Subcutaneous nodules.
6.6. Serum rheumatoid factor.Serum rheumatoid factor.
7.7. Radiological changes ( erosion ).Radiological changes ( erosion ).
Duration of (1,2,3,4) for 6 weeks or more.Duration of (1,2,3,4) for 6 weeks or more.

Extra-articular manifestations.Extra-articular manifestations.
A.A. In soft tissue surrounding joints.In soft tissue surrounding joints.
1.1. Rheumatoid nodules.( found in 20—30% ) ,Rheumatoid nodules.( found in 20—30% ) ,
mostly in seropositsve . Are subcutaneous, notmostly in seropositsve . Are subcutaneous, not
attached to skin or underlying tissue, mobile ,attached to skin or underlying tissue, mobile ,
not tender & located on extensor surface ofnot tender & located on extensor surface of
elbow , forearm, wrist , occiput& achills tendon.elbow , forearm, wrist , occiput& achills tendon.
Might be found in chest , heart or eye.Might be found in chest , heart or eye.

2.2. Bursitis. Olrcranon or other bursae.Bursitis. Olrcranon or other bursae.
3.3. Tenosynovitis. ( flexor tendons in palm—TriggerTenosynovitis. ( flexor tendons in palm—Trigger
finger).finger).
4.4. Muscle wasting. As in small muscles of hands.Muscle wasting. As in small muscles of hands.
5.5. Cyst & repture joints.( baker s cyst).Cyst & repture joints.( baker s cyst).

B.B. The eyes.The eyes.
1.1. Insuffecient secretion ( dry eye –Insuffecient secretion ( dry eye –
Keratoconjunctivitis sicca – Sjogrens syndrome)Keratoconjunctivitis sicca – Sjogrens syndrome)
2.2. Scleritis,Scleritis,
3.3. Episcleritis.Episcleritis.

C.C. The nervous system.The nervous system.
1.1. Peripheral neuropathy.Peripheral neuropathy.
A.A. Polyneuropathy( rare causing glove & stocking)Polyneuropathy( rare causing glove & stocking)
B.B. Entrapment neuropathy ( CTS ).Entrapment neuropathy ( CTS ).
2.2. Atlanto-axial sublaxation.Atlanto-axial sublaxation.

D.D. The spleen, lymph nodes & blood.The spleen, lymph nodes & blood.
1.1. Palpable lymph nodes are common.Palpable lymph nodes are common.
2.2. Spleen may be enlarged.Spleen may be enlarged.
3.3. Felty syndrome{ arthritis(RA) , splenomegaly &Felty syndrome{ arthritis(RA) , splenomegaly &
neutropenia.}neutropenia.}
4.4. Aanaemia is almost universal ( nomochromicAanaemia is almost universal ( nomochromic
nomocytic type).nomocytic type).
NSAIDs might cause it.NSAIDs might cause it.

E.E. Blood vessels & heart.Blood vessels & heart.
 Vasculitis might occur in RA. ( tinny spotsVasculitis might occur in RA. ( tinny spots
around finger nails,around finger nails,
 Raynuds phenomenon but gangrene could occur)Raynuds phenomenon but gangrene could occur)
 PericarditisPericarditis
 MyocarditisMyocarditis
 Conduction defectsConduction defects
 EndocarditisEndocarditis

F. Respiratory system.F. Respiratory system.
 RA in pleura or lunge.RA in pleura or lunge.
 Pleural effusion.Pleural effusion.
 Fibrosing alveolitis.Fibrosing alveolitis.
 Caplans lung.Caplans lung.

G. The kidneys.G. The kidneys.
 Effecct of NSAIDs.Effecct of NSAIDs.
 Amyloidosis.( Nephrotic syndrome).Amyloidosis.( Nephrotic syndrome).
 RA predispose to infection.sRA predispose to infection.s

A.A. Laboratory testsLaboratory tests
1.1. Anaemia. ( of chronic diseasea), elevation ofAnaemia. ( of chronic diseasea), elevation of
ESR , leucocytosis ( may be) , thrombocytosis.ESR , leucocytosis ( may be) , thrombocytosis.
2.2. Rheumatoid factor is positsve in 75- 80% ofRheumatoid factor is positsve in 75- 80% of
cases.cases.
3.3. ANA is positive in 20- 40 % .ANA is positive in 20- 40 % .
4.4. Synovial fluid is of inflammatory type.( WBCSynovial fluid is of inflammatory type.( WBC
30.000/ cc).30.000/ cc).

B.B. Radiology.Radiology.
1.1. Soft tissue swelling.Soft tissue swelling.
2.2. Periarticular osteoporosis.Periarticular osteoporosis.
3.3. Marginal erosion.Marginal erosion.
Later.Later.
4.4. Decrease joint space.Decrease joint space.
5.5. More extensive erosion.More extensive erosion.
6.6. Joint sublaxation & dislocation.Joint sublaxation & dislocation.
7.7. Ankylosis.Ankylosis.

Course & prognosis & causes of death.Course & prognosis & causes of death.
1.1. 20% might improve spontaneously20% might improve spontaneously..
2.2. A small group develop very sever form (A small group develop very sever form (
malignant or fulminating RA)malignant or fulminating RA)
3.3. Infection ( pyoarthrosis or septicaemia).Infection ( pyoarthrosis or septicaemia).
4.4. Cricoaretenoid arthritis.Cricoaretenoid arthritis.
5.5. Atlantoaxial sublaxation.Atlantoaxial sublaxation.
6.6. From hazards of drug therapy.From hazards of drug therapy.
7.7. Amyloidosis.Amyloidosis.

TreatmentTreatment
Treatment is comprehensive ( Medical ,Treatment is comprehensive ( Medical ,
Rehabilitative & Surgical ).Rehabilitative & Surgical ).
Aims are :Aims are :
1.1. Education & motivation of the patient .Education & motivation of the patient .
2.2. Relief of pain.Relief of pain.
3.3. Induction of remission.Induction of remission.
4.4. Maintinance of joint function.Maintinance of joint function.
5.5. Avoid & recognize side effects early.Avoid & recognize side effects early.
6.6. Preserve or restore function.Preserve or restore function.
7.7. Maintain life style.Maintain life style.

Drug therapy.Drug therapy.
1.1.AnalgesiaAnalgesia..
2.2.NSAIDs.NSAIDs.
3.3. Disease modifying antirheumatic drugs.Disease modifying antirheumatic drugs.
a.a. Gold salts( injectable—sodium aurothiomalate orGold salts( injectable—sodium aurothiomalate or
oral one auranofine ).oral one auranofine ).
b.b. D-penecillamine.D-penecillamine.
c.c. Antimalarials ( Chloroquine & Hydroxychloroquine).Antimalarials ( Chloroquine & Hydroxychloroquine).
d.d.Methtrexate.Methtrexate.
e.e. Sulfasalzine.Sulfasalzine.
f.f.Leflunomide.Leflunomide.
Some other cytotoxic drugs like Azathioprine orSome other cytotoxic drugs like Azathioprine or
Chlorambucile ---etc—could be used.Chlorambucile ---etc—could be used.

4.4. Biologic agents ( Tumor necrosis factorBiologic agents ( Tumor necrosis factor
inhibitors –Infleximab & Etanercept ).inhibitors –Infleximab & Etanercept ).
5.5. Steroids ( systemic or local).Steroids ( systemic or local).
6.6. Combination therapy.Combination therapy.

Course & prognosis.Course & prognosis.
The course is variable;The course is variable;
1.1. 25% remaine fit for all activities.25% remaine fit for all activities.
2.2. 40% develop moderate disability.40% develop moderate disability.
3.3. 25% are quit badly disabled.25% are quit badly disabled.
4.4. 10% become wheelchair bound.10% become wheelchair bound.

Poor prognosis is indicated by:Poor prognosis is indicated by:
1.1. High titre rheumatoid factor.High titre rheumatoid factor.
2.2. Early appearance of erosion.Early appearance of erosion.
3.3. Rheumatoid nodules.Rheumatoid nodules.
4.4. Systemic manifestations.Systemic manifestations.
5.5. Presence of HLADR4.Presence of HLADR4.
6.6. Extraarticular manifestations.Extraarticular manifestations.
7.7. Sever functional impairment.Sever functional impairment.
8.8. Continues active disease.( Remission is better ).Continues active disease.( Remission is better ).

Juvenile Rheumatoid ArthritisJuvenile Rheumatoid Arthritis
This is a term used to describe a group of chronic
arthritidies that affect children( under age of 16
years) .

Classification.Classification.
1.1. Systemic JCA ( Jevenile chronic arthritis).Systemic JCA ( Jevenile chronic arthritis).
2.2. Pauciarticular JCA.Pauciarticular JCA.
A-A- Young girls .Young girls .
B-B- Older boys ( HLA B27).Older boys ( HLA B27).
3.3. Polyarticular onset ( sero_ Negative & sero + ) .Polyarticular onset ( sero_ Negative & sero + ) .

Characters.Characters.
1.1. Starts befor age of 16 y.Starts befor age of 16 y.
2.2. Lasts at least 3 months.Lasts at least 3 months.
3.3. 1/ 2000 of population are at risk.1/ 2000 of population are at risk.
4.4. Most are seronegative for IgM.Most are seronegative for IgM.
5.5. Peak onset is at 2_ 4 years of age with anotherPeak onset is at 2_ 4 years of age with another
smaller peak at puberty.smaller peak at puberty.

Systemic onsetSystemic onset
This type makes about 20% of JCA .This type makes about 20% of JCA .
1.1.It occurs under 5 y. of age.It occurs under 5 y. of age.
2.2. Fever & rash are main features.Fever & rash are main features.
3.3. Has prominent extrarticular features.Has prominent extrarticular features.
( lymphadenopathy, splenomegaly, hepatomegaly ,( lymphadenopathy, splenomegaly, hepatomegaly ,
pericarditis, pleurisy & abdominal pain).pericarditis, pleurisy & abdominal pain).

Pauciarticular .Pauciarticular .
This account for about 40% of JCA.This account for about 40% of JCA.
1.1.Female predominance ( usually positive for ANAFemale predominance ( usually positive for ANA
but not RA factor).( there is a risk of iridocyclitis &but not RA factor).( there is a risk of iridocyclitis &
blindness).Have HLADR5 , HLADR8 .blindness).Have HLADR5 , HLADR8 .
Knees , ankles & wrists are frequently affected.Knees , ankles & wrists are frequently affected.
2.2. 2nd type has strong male predominance , later2nd type has strong male predominance , later
age onset & majority has HLAB27 & graduallyage onset & majority has HLAB27 & gradually
evolves to AS.evolves to AS.

Pauci articular JRAPauci articular JRA

Polyarticular onset.Polyarticular onset.
Account for 40% of cases.Account for 40% of cases.
Females are more affected .Females are more affected .
About 10% of these are seo + which has worstAbout 10% of these are seo + which has worst
prognosis.prognosis.

There is nonabsolut diagnostic test.There is nonabsolut diagnostic test.
ESR is elevated in the active phase,ESR is elevated in the active phase,
WBC count might be high,WBC count might be high,
ANF is present in 30% of cases & RA factorANF is present in 30% of cases & RA factor
in adult type .in adult type .

X_ ray changes are mainly periarticularX_ ray changes are mainly periarticular
osteoporosis & periosteitis around joints.osteoporosis & periosteitis around joints.
In younger children premature appearance ofIn younger children premature appearance of
epiphysis & in older ones premature fusion ofepiphysis & in older ones premature fusion of
epiphysis are features. Erosion is mainly seen inepiphysis are features. Erosion is mainly seen in
sero+ group & comes late in other types.sero+ group & comes late in other types.

M anagement.M anagement.
Aims.Aims.
1.1.Suppress & control the disease activity.Suppress & control the disease activity.
2.2.Prevent deformities.Prevent deformities.
3.3. Help the child to live a normal life.Help the child to live a normal life.
Rest & proper positioning in acute phase.Rest & proper positioning in acute phase.
Start physiotherapy program once the child as soonStart physiotherapy program once the child as soon
as the child is ready. Splint(s) could be used.as the child is ready. Splint(s) could be used.
Suppression of activity.Suppression of activity.
Drugs are more or less are those used in adult RA.Drugs are more or less are those used in adult RA.
NSAID are used.NSAID are used.
DMARD are used ( Gold , methotrexate ) .DMARD are used ( Gold , methotrexate ) .
Steroids are sometimes used ( systemic & local ).Steroids are sometimes used ( systemic & local ).
Surgery is restricted to synovectomy, correction ofSurgery is restricted to synovectomy, correction of
deformities and joint replacement ( hip).deformities and joint replacement ( hip).

Seronegative spondarthritides.Seronegative spondarthritides.
Are a group of hetrogenous disordersAre a group of hetrogenous disorders
charecterised by :charecterised by :
1.1. Constant absence of IgM rheumatoid serumConstant absence of IgM rheumatoid serum
factor.factor.
2.2. Involvment of axial skeleton.Involvment of axial skeleton.
3.3. Peripheral joint involvement.Peripheral joint involvement.
4.4. Clinical evidence of overlap exist between them.Clinical evidence of overlap exist between them.
5.5. Basic pathological changes isBasic pathological changes is
ENTHESOPATHY.ENTHESOPATHY.
6.6. Tendency for familial aggregation ( HLA B27).Tendency for familial aggregation ( HLA B27).

This group consist of:This group consist of:
1.1. AS.AS.
2.2. Psoriatc arthritis.Psoriatc arthritis.
3.3. Enteropathic arthritis.Enteropathic arthritis.
4.4. Reiter s syndrome.Reiter s syndrome.
5.5. Juvenile onset spondylarthropathyJuvenile onset spondylarthropathy
6.6. Undifferentiated spondylarthropathy.Undifferentiated spondylarthropathy.
7.7.Behcet s disease ?]Behcet s disease ?]

The common features are:The common features are:
1.1. Negative test for IgM rheumatoid factor.Negative test for IgM rheumatoid factor.
2.2. Absence of rheumatoid nodules.Absence of rheumatoid nodules.
3.3. Asymmetrical peripheral arthritis.Asymmetrical peripheral arthritis.
4.4. Radiological sacroilitis.Radiological sacroilitis.
5.5. Evidence of clinical overlap between them.Evidence of clinical overlap between them.
6.6. Tendency to familial aggregation.Tendency to familial aggregation.

Diagnostic criteria for diagnosis ofDiagnostic criteria for diagnosis of
spondylarthropathies by Amor ( 1993).spondylarthropathies by Amor ( 1993).
1. Lumbar pain at night or morning stiffness( 1 ).
2. Asymmetrical oligoarthritis ( 2 ).
3. Buttock pain ( 2 ).
4. Alternating buttock pain ( 2 ).
5. Susage like toe or digits ( 2 ).

6. Heel pain or enthesis ( 2 ).
7. Iritis ( 2 ).

8.8. Nongonococcal urethritis , cervicitis within oneNongonococcal urethritis , cervicitis within one
month of onset (1).month of onset (1).
9.9. Acute diarrhea within one month of arthriticAcute diarrhea within one month of arthritic
onset (1).onset (1).
10.10. Psoriasis , balanitis or inflammatory bowelPsoriasis , balanitis or inflammatory bowel
disease (1).disease (1).
11.11. Sacroiliitis (2).Sacroiliitis (2).
12.12. Positive test for HLA B27 or positive familyPositive test for HLA B27 or positive family
history for spodylarthropathy.(2)history for spodylarthropathy.(2)
13.13. Rapid response to NSAIDs ( within 48 hours )Rapid response to NSAIDs ( within 48 hours )
(2).(2).
Diagnosis require score more than ( 6 ) scors.Diagnosis require score more than ( 6 ) scors.

Ankylosing Spondylitis.Ankylosing Spondylitis.
AS is an inflammatory disorder of unknownAS is an inflammatory disorder of unknown
aetiology that primarily affecting axialaetiology that primarily affecting axial
skeleton & large proximal joints.skeleton & large proximal joints.

Epidemiology & Aetiology.Epidemiology & Aetiology.
AS shows a striking correlation with HLA B27. It s a world
wide disease.
HLA B27 is found in 10 to 20% among first degree relatives
of of AS patients While it is found in 50% of identical
twins of AS patients.
An abnormal response to Klebsiela which carry an antigen
mimics B27 has been suggested as underlying cause of
AS.
These findings indicate that both genetic &environmental
factors play role in pathogenesis of AS.

1.1. The basic pathological lesion is ENTHESOPATHY.The basic pathological lesion is ENTHESOPATHY.
2.2. The process usually starts from Sacroiliac joints.( lowerThe process usually starts from Sacroiliac joints.( lower
part).part).
3.3. the early lesion is subchondral granulation tissuethe early lesion is subchondral granulation tissue
( lymphocyte, plasma cells, mast cells macrophage &( lymphocyte, plasma cells, mast cells macrophage &
chondrocytes). Usually starts from the lower 2/3chondrocytes). Usually starts from the lower 2/3
synovial part of sacroiliac joint & thinner iliacsynovial part of sacroiliac joint & thinner iliac
cartilagecartilage
is first affected.is first affected.
4.4. The inflamed joint margin become widened , irregularThe inflamed joint margin become widened , irregular
later on calcified( ossified) ultimately the joint may belater on calcified( ossified) ultimately the joint may be
totally obliterated.totally obliterated.

5.5. In the spine ( Squering of vertebrae ossification ofIn the spine ( Squering of vertebrae ossification of
outer most fibers of annulas fibrosus, syndesmophytesouter most fibers of annulas fibrosus, syndesmophytes
& eventually Bamboo spine).& eventually Bamboo spine).
Diffuse osteoporosis of the spine could occur, erosionDiffuse osteoporosis of the spine could occur, erosion
and sclrerosis of verteberal bodies at disk margine ,and sclrerosis of verteberal bodies at disk margine ,
squaring of vertebrae & inflammation & destruction ofsquaring of vertebrae & inflammation & destruction of
disk_ bone border . Inflammatory arthritis of thedisk_ bone border . Inflammatory arthritis of the
apophysial joints is common.apophysial joints is common.
6.6. Inflammatory arthritis might occur in peripheral jointsInflammatory arthritis might occur in peripheral joints
( hip is commonest ).( hip is commonest ).
7.7. Enthesopathy ( plantar fasciitis, tennis elbow etc….).Enthesopathy ( plantar fasciitis, tennis elbow etc….).

8.8.Other cartiligenous joints i.e Sternomnibural &Other cartiligenous joints i.e Sternomnibural &
pubic symphysis could be affected.pubic symphysis could be affected.
9.9.Eyes ( anterior uveitis ( iritis) occurs in 20% ofEyes ( anterior uveitis ( iritis) occurs in 20% of
cases.cases.
10.10.Aortic insufficiency occurs in small number ofAortic insufficiency occurs in small number of
cases.cases.
11.11.Microscopical inflammatory lesions of colon &Microscopical inflammatory lesions of colon &
ileocecal valve have been found in 25__ 50% ofileocecal valve have been found in 25__ 50% of
patients even without clinical evidence ofpatients even without clinical evidence of
inflammatory bowel disease.inflammatory bowel disease.

Clinical Manifestations.Clinical Manifestations.
Age onset is 16—40 y.Age onset is 16—40 y.
Male / female is 2—3 / 1.Male / female is 2—3 / 1.
Onset is insidious.Onset is insidious.
Low back pain & stiffness are the usual presentingLow back pain & stiffness are the usual presenting
symptoms.symptoms.
1.1.The pain is insidious & dull ache in nature , feltThe pain is insidious & dull ache in nature , felt
deep in the lower lumber & gluteal region ( sacroiliacdeep in the lower lumber & gluteal region ( sacroiliac
region).region).
2.2.Morning stiffness up to few hours.Morning stiffness up to few hours.

3.3.Might have constitutional symptoms.Might have constitutional symptoms.
4.4. Symtoms are initially usually episodic.Symtoms are initially usually episodic.
5.5. Nocturnal exacerbation that make the patient toNocturnal exacerbation that make the patient to
walk around.walk around.
6.6. Tender lower back.Tender lower back.

7.7.Decrease spinal movement in all directionsDecrease spinal movement in all directions
which spreads up to thoracic & cervical regions.which spreads up to thoracic & cervical regions.
8.8. Enthesopathy ( plantar fasciitis , tennis elbowEnthesopathy ( plantar fasciitis , tennis elbow
etc….).etc….).
9.9. Occasionally boney chest pain is a presentingOccasionally boney chest pain is a presenting
symptom.symptom.
10.10. Involvement of costovertebral joint results inInvolvement of costovertebral joint results in
the reduction of chest expansion.the reduction of chest expansion.

11.11.Peripheral asymmetrical arthritis might occurPeripheral asymmetrical arthritis might occur
( hip is commonest ).( hip is commonest ).
12.12. Eye ivolvement occur in 40% of cases.Eye ivolvement occur in 40% of cases.
13.13. Aortic insufficiency might produce heartAortic insufficiency might produce heart
failure.failure.
14.14.In lunge apical fibrosis & cavitation mightIn lunge apical fibrosis & cavitation might
occur.occur.

Physical signs:Physical signs:
1.1. Decrease spinal movments ( schober test)Decrease spinal movments ( schober test)
2.2. Tender SI joints .Tender SI joints .
3.3. Decrease chest expansion.Decrease chest expansion.
4.4. Decrease hip movments.Decrease hip movments.
5.5. Kyphosis in thoracic spine & reduced lumbarKyphosis in thoracic spine & reduced lumbar
lordosis.lordosis.
6.6. Atrophy of buttocks muscles.Atrophy of buttocks muscles.

ESR is elevated in acute phase & so C reactiveESR is elevated in acute phase & so C reactive
proteinprotein
Normochoromic normocytic anemia .Normochoromic normocytic anemia .
Alkaline phosphates & IgG might be high.Alkaline phosphates & IgG might be high.
HLAB27 is present in above 90% of cases.HLAB27 is present in above 90% of cases.

Radiology ( imagingRadiology ( imaging ).).
MRI & CT scan are showing changes beforeMRI & CT scan are showing changes before
conventional x—ray.conventional x—ray.
A. Radiological changes in S.I joints are :A. Radiological changes in S.I joints are :
1.1. Blurring of subcortical margine ofBlurring of subcortical margine of
subchondral bone.subchondral bone.
2.2. Erosions & sclerosis.Erosions & sclerosis.
3.3. Pseudowidnening of the joint.Pseudowidnening of the joint.
4.4. Boney ankylosis.Boney ankylosis.

Normal SI joint Sacro ilitisNormal SI joint Sacro ilitis

B.B. In the spine.In the spine.
1.1. Squaring of vertebra.Squaring of vertebra.
2.2. Ossification of outer layer of annulasOssification of outer layer of annulas
firosus.firosus.
3.3. Marginal syndesmophyte.Marginal syndesmophyte.
4.4. Bamboo spine.Bamboo spine.

Treatment.Treatment.
The principles are:The principles are:
1.1. Relief pain.Relief pain.
2.2. Proper positioning.Proper positioning.
3.3. Exercise program to maintain mobility &Exercise program to maintain mobility &
preserve range of motion.preserve range of motion.

Drug therapy:Drug therapy:
1.1. NSAIDs.( Indomthacine, phenylbutazone canNSAIDs.( Indomthacine, phenylbutazone can
be used ).be used ).
2.2. Sulfasalzine & MTX are used when there isSulfasalzine & MTX are used when there is
peripheral joint involvement.( used in spinalperipheral joint involvement.( used in spinal
involvement).involvement).
3.3. Tumor necrosis factor inhibitors are effectiveTumor necrosis factor inhibitors are effective
( Infleximab or Etanercept)( Infleximab or Etanercept)
4.4. Systemic steroid might be used ( intractableSystemic steroid might be used ( intractable
uveitis )uveitis )
5.5. Local steroid to affected joints could be usedLocal steroid to affected joints could be used
( CT guided for SI joints).( CT guided for SI joints).

Psoriatic ArthritisPsoriatic Arthritis
PsA is a chronic disease sero-negativePsA is a chronic disease sero-negative
inflammatory arthritis that affects 5_7% of peopleinflammatory arthritis that affects 5_7% of people
with cutaneous psoriasis.with cutaneous psoriasis.
In adults it mostly occurs in patients with activeIn adults it mostly occurs in patients with active
cutaneous disease while in children the jointcutaneous disease while in children the joint
manifestations might antedate articular features.manifestations might antedate articular features.
The extend of psoriatic skin disease correlatesThe extend of psoriatic skin disease correlates
poorly with the onset of arthritis , the risk of PsApoorly with the onset of arthritis , the risk of PsA
increases with family history of spondylarthropathyincreases with family history of spondylarthropathy
or extensive nail pitting.or extensive nail pitting.

Aetiology & Pathogenesis.Aetiology & Pathogenesis.
The cause & pathogenesis of PsA is unknown .The cause & pathogenesis of PsA is unknown .
There is a strong evidence of genetic influence inThere is a strong evidence of genetic influence in
the disease over 30% having family history of thethe disease over 30% having family history of the
disorder there is an increased frequency ofdisorder there is an increased frequency of
( HLA_B17 , CW6, DQ2 &/ or HLA_B27) in( HLA_B17 , CW6, DQ2 &/ or HLA_B27) in
patients with psoriatic spondylitis while B27, BW62patients with psoriatic spondylitis while B27, BW62
, B38, B39 & DR7 have noted in association with, B38, B39 & DR7 have noted in association with
peripheral arthritis .peripheral arthritis .
Fulminating cases should make on suspect humanFulminating cases should make on suspect human
immunodeficiency virus disease ( HIV ).immunodeficiency virus disease ( HIV ).
Trauma & infection suggested to increase cellularTrauma & infection suggested to increase cellular
immunity ( i.e streptococcus) may each play aimmunity ( i.e streptococcus) may each play a

PsA has an insidious onset & progressivePsA has an insidious onset & progressive
course.course.
The onset of arthritis is usually preceded byThe onset of arthritis is usually preceded by
skin disease but may accompany it or theskin disease but may accompany it or the
arthritis may preced the skin lesion ( as inarthritis may preced the skin lesion ( as in
children).children).

There are at least five clinical subsets.sThere are at least five clinical subsets.s
1.1. Asymmetric oligoarthritis : CharacterisedAsymmetric oligoarthritis : Characterised
by asymmetric involvement of both largeby asymmetric involvement of both large
& small joints & the appearance of susage& small joints & the appearance of susage
_ shaped digits is common. This subset is_ shaped digits is common. This subset is
making about 30__50 % of patients , theremaking about 30__50 % of patients , there
is a little relationship between the joint &is a little relationship between the joint &
skin activity.skin activity.

2.2. Involvment of DIP joints. Is seen in 10%Involvment of DIP joints. Is seen in 10%
of cases it is strongly associated with nailof cases it is strongly associated with nail
changes of pitting , onycolysis , subungalchanges of pitting , onycolysis , subungal
keratosis &Ridging.keratosis &Ridging.

Psoriatic arthritis with distal joint involvement inPsoriatic arthritis with distal joint involvement in
the third and fifth digits (arrow). Onycholysis is alsothe third and fifth digits (arrow). Onycholysis is also
seen in most of the fingernails.seen in most of the fingernails.

4.4. Psoriatic spondylitis : is making about 20%Psoriatic spondylitis : is making about 20%
of PsA , 50% are having HLA_B27 , theyof PsA , 50% are having HLA_B27 , they
have sacroiliitis .have sacroiliitis .
There is malepredominance.There is malepredominance.

3.3. Symmetric polyarthritis : Resembling RA.Symmetric polyarthritis : Resembling RA.

5.5. Arthritis mutilance : There is a severeArthritis mutilance : There is a severe
destructive arthropathy resulting indestructive arthropathy resulting in
mutilation of joints & telescoping digits tomutilation of joints & telescoping digits to
produce the so called opera glass hand.produce the so called opera glass hand.

Skin & nail changes.Skin & nail changes.
Psoriatic lesions are typically occur on thePsoriatic lesions are typically occur on the
scalp , elbow,behind ears & knees.scalp , elbow,behind ears & knees.

Nail changes include small pits , onycolysis,Nail changes include small pits , onycolysis,
subungual keratosis , thickening &subungual keratosis , thickening &
distortion of nail with ridging. Presence ofdistortion of nail with ridging. Presence of
20 pits in total is suggestive of psoriasis20 pits in total is suggestive of psoriasis
while presence of more than 60 pits beenwhile presence of more than 60 pits been
diagnostic.diagnostic.

This photograph of the hand of a patient with psoriaticThis photograph of the hand of a patient with psoriatic
arthritis shows characteristic early nail separationarthritis shows characteristic early nail separation
(onycholysis), swelling and erythema of the index and little(onycholysis), swelling and erythema of the index and little
finger distal interphalangeal joints.finger distal interphalangeal joints.

1.1. Elevated ESRin 1/3 of cases, C—reactive protein &Elevated ESRin 1/3 of cases, C—reactive protein &
complement levels reflect inflammation.complement levels reflect inflammation.
2.2. Rheumatoid factors are absent.Rheumatoid factors are absent.
3.3. Mild normochromic normocytic anemia is seen inMild normochromic normocytic anemia is seen in
chronic cases.chronic cases.
4.4. Immunological levels esoecially IgA level may beImmunological levels esoecially IgA level may be
elevated.elevated.
5.5. Synovial fluid is of inflammatory type.Synovial fluid is of inflammatory type.
6.6. ANA could be positive in low titre & anti dsDNAANA could be positive in low titre & anti dsDNA
in 3% of cases.in 3% of cases.
7.7. AntiCCP could be positiove in 8—16% .AntiCCP could be positiove in 8—16% .

8.8. Radiology.Radiology.
Soft tissue swelling , loss of cartilage space,Soft tissue swelling , loss of cartilage space,
erosion , boney ankylosis of fingers , sublaxation &erosion , boney ankylosis of fingers , sublaxation &
subchondral bone cyst. There is less bonesubchondral bone cyst. There is less bone
demineralization. More unique & suggestive ofdemineralization. More unique & suggestive of
PsA arthritis are erosion of DIP joints , expansionPsA arthritis are erosion of DIP joints , expansion
of base of terminal phalanx & terminal phalangealof base of terminal phalanx & terminal phalangeal
osteolysis ( reabsorption).osteolysis ( reabsorption).

The axial skeleton shows asymmetric or unilateralThe axial skeleton shows asymmetric or unilateral
sacroiliitis , often a symptomtic paravertebralsacroiliitis , often a symptomtic paravertebral
ossification including cervical spine & largeossification including cervical spine & large
asymmetric nonmarginal osteophytes.asymmetric nonmarginal osteophytes.

Diagnosis of of PsA depends on finding typical cutaneous or nailDiagnosis of of PsA depends on finding typical cutaneous or nail
changes in association with one of recognized articular variantschanges in association with one of recognized articular variants..
Psoriatic arthritis associated with pencil-in-cup abnormality in thePsoriatic arthritis associated with pencil-in-cup abnormality in the
distal interphalangeal (DIP) joints of the first and second fingersdistal interphalangeal (DIP) joints of the first and second fingers
(short arrows), plus early changes in the DIP joint of the fourth(short arrows), plus early changes in the DIP joint of the fourth
finger. Other changes include ankylosis in the DIP joint in the fifthfinger. Other changes include ankylosis in the DIP joint in the fifth
finger (long arrow) and destruction of the wrist.finger (long arrow) and destruction of the wrist.

TreatmentTreatment..
1.1. NSAIDs.NSAIDs.
2.2. DMARD ( Sulfasalazine , gold , D_ penicillamin &DMARD ( Sulfasalazine , gold , D_ penicillamin &
Methotrexate ) could be used , while the use ofMethotrexate ) could be used , while the use of
antimaliarials is controversial . MTX is particularlyantimaliarials is controversial . MTX is particularly
effective in managing the skin & joint disease.effective in managing the skin & joint disease.
3.3. Itra-articular steroid could be used in absence ofItra-articular steroid could be used in absence of
psoriatic lesions around the joint injected.psoriatic lesions around the joint injected.
4.4. Systemic steroid is better to be avoided since taperingSystemic steroid is better to be avoided since tapering
tends to cause an exacerbation of the skin lesion.tends to cause an exacerbation of the skin lesion.
5.5. Azathioprin may be used .Azathioprin may be used .
6.6. Spinal disease is treated as AS.Spinal disease is treated as AS.
7.7. Biological agents could be used.Biological agents could be used.
In most cases the prognosis is good & joint function isIn most cases the prognosis is good & joint function is
preserved or slightly impaired , but deformity &preserved or slightly impaired , but deformity &
disability occur in some patients.disability occur in some patients.

Reactive Arthritis.Reactive Arthritis.
Is refers to occurance of an acute nonsuppurativeIs refers to occurance of an acute nonsuppurative
, sterile inflammatory arthropathy arising after an, sterile inflammatory arthropathy arising after an
infectious process but at a site remote from theinfectious process but at a site remote from the
primary infection.primary infection.
The microbial pathogens commonly associatedThe microbial pathogens commonly associated
with reactive arthritis are shigella , salmonella ,with reactive arthritis are shigella , salmonella ,
yersenia & Chlamydia.yersenia & Chlamydia.

Many reactive arthritis occur after a knownMany reactive arthritis occur after a known
infection & therefore have named post_ infection.infection & therefore have named post_ infection.
Reactive arthritis begins as asymmetricalReactive arthritis begins as asymmetrical
oligoarthritis often precede by an identifiableoligoarthritis often precede by an identifiable
infectious event by one to four weeks.infectious event by one to four weeks.
The common example of reactive arthritis isThe common example of reactive arthritis is
Reiter’ s syndrome.Reiter’ s syndrome.

COURSE AND PROGNOSISCOURSE AND PROGNOSIS
In general, reactive arthritis follows one of fourIn general, reactive arthritis follows one of four
courses after the initial acute attack .courses after the initial acute attack .
1.1. The arthritis attack is self-limiting and mayThe arthritis attack is self-limiting and may
never recur, with a duration usually less than sixnever recur, with a duration usually less than six
months (35 percent). Pain at themonths (35 percent). Pain at the
metatarsophalangeal joints and the heels mightmetatarsophalangeal joints and the heels might
remain painful for months. Approximately 75remain painful for months. Approximately 75
percent of patients are in complete remission afterpercent of patients are in complete remission after
two years.two years.
2.2. The disease goes into remission but recursThe disease goes into remission but recurs
intermittently (35 percent). The recurrence mightintermittently (35 percent). The recurrence might
only be an arthritis, an enthesopathy, or be foundonly be an arthritis, an enthesopathy, or be found
in an extraarticular location.in an extraarticular location.

3.3. The attack never subsides completely butThe attack never subsides completely but
continues with a waxing and waning coursecontinues with a waxing and waning course
(25 percent).(25 percent).
4.4. A few patients continue to have severeA few patients continue to have severe
inflammatory disease for many years and mayinflammatory disease for many years and may
even develop features of destructive arthritis ineven develop features of destructive arthritis in
multiple joints or the diffuse spinal changes ofmultiple joints or the diffuse spinal changes of
ankylosing spondylitis (5 percent).ankylosing spondylitis (5 percent).

Reiter’s SyndromeReiter’s Syndrome
This syndrome consists of the triad ofThis syndrome consists of the triad of
 seronegative reactive arthritisseronegative reactive arthritis
 nonspecific uerethritisnonspecific uerethritis
 ConjunctivitisConjunctivitis
( this traid is only observed in 33% of patients ),( this traid is only observed in 33% of patients ),
many patients will not have prodromal enteric ormany patients will not have prodromal enteric or
urethral inflammation such patients areurethral inflammation such patients are
designated as incomplete Reiter’s.designated as incomplete Reiter’s.
When arthritis alone follows sexual exposure orWhen arthritis alone follows sexual exposure or
enteric infection the term reactive arthritis isenteric infection the term reactive arthritis is
frequently used.frequently used.

Clinical FeaturesClinical Features
The earlest features of RS frequently appear withinThe earlest features of RS frequently appear within
1__4 weeks of Putative microbial exposure.1__4 weeks of Putative microbial exposure.
Disease onset is usually heralded by developmentDisease onset is usually heralded by development
of one or of the extraarticular feature.of one or of the extraarticular feature.
The diagnostic traid in RS is (urethritisThe diagnostic traid in RS is (urethritis
,conjunctivitis & arthritis ) one of this triad may,conjunctivitis & arthritis ) one of this triad may
be absent.be absent.
Urethritis can occur in the postdysentric form of theUrethritis can occur in the postdysentric form of the
disease & the reverse is also possible.disease & the reverse is also possible.
Age range is 16__ 35 Y, male / female is 20 / 1 inAge range is 16__ 35 Y, male / female is 20 / 1 in
post-urethritic infection , while it has an equal sexpost-urethritic infection , while it has an equal sex
distribution in post-dysenteric one.distribution in post-dysenteric one.

ArthritisArthritis ::
Is often the last feature to appear , it is sero-Is often the last feature to appear , it is sero-
negative mono or oligoarthritis affecting weightnegative mono or oligoarthritis affecting weight
bearing joints ( knees, metatarsophalangeal ,bearing joints ( knees, metatarsophalangeal ,
ankles or interphalangeal joints ). In half of theankles or interphalangeal joints ). In half of the
cases the onset is acute ( acute arthritis withcases the onset is acute ( acute arthritis with
effusion ). The severity of arthritis is varies fromeffusion ). The severity of arthritis is varies from
mild transient to chronic destructive .mild transient to chronic destructive .
Enthesitis is might be a feature .Enthesitis is might be a feature .
Sacroiliitis & spondylitis occur in about 50% ofSacroiliitis & spondylitis occur in about 50% of
cases & lead to backache( with radiologicalcases & lead to backache( with radiological
changes in chronic cases ).changes in chronic cases ).

ACR criteria for diagnosis require the presence ofACR criteria for diagnosis require the presence of
peripheral arthritis of more than one monthperipheral arthritis of more than one month
duration occurring in association with urethritisduration occurring in association with urethritis
&/ or cervicitis.&/ or cervicitis.
Isolated involvement of lumbar & thoracic spineIsolated involvement of lumbar & thoracic spine
could be an initial radiographic findings &could be an initial radiographic findings &
involvement of cervical spine is uncommon.involvement of cervical spine is uncommon.

Urethritis :Urethritis :
is nongonococcal , is usually the first feature ,is nongonococcal , is usually the first feature ,
manifests as a clear sterile discharge withmanifests as a clear sterile discharge with
minimal dysuria , it might be asymptomatic .minimal dysuria , it might be asymptomatic .
Occasionally it is sever.Occasionally it is sever.
Occlar lesion :Occlar lesion :
Bilateral sterile conjunctivitis is the most commonBilateral sterile conjunctivitis is the most common
form & is usually mild but occasionally may beform & is usually mild but occasionally may be
sever with almost all parts of the eye involved.sever with almost all parts of the eye involved.

Mucocutaneous lesions :Mucocutaneous lesions :
Features may affect the GU or GI tracts . In GU areFeatures may affect the GU or GI tracts . In GU are
( transient mucopurulent discharge , urethritis,( transient mucopurulent discharge , urethritis,
circnate balanitis appears as painless vesicls orcircnate balanitis appears as painless vesicls or
large, shallow, serpiginous ulceration or plaqueslarge, shallow, serpiginous ulceration or plaques
on the glans or shaft of the penis .on the glans or shaft of the penis .
Painless lingual, palatal & oral ulceration may bePainless lingual, palatal & oral ulceration may be
seen in up to 50% of patients.seen in up to 50% of patients.
Keratdermia blennorrhagica ( is painlessKeratdermia blennorrhagica ( is painless
papulosquematous eruption frequently found onpapulosquematous eruption frequently found on
the sole or palm, it heals without leaving scar ).the sole or palm, it heals without leaving scar ).
Patients with chronic disease might demonstratePatients with chronic disease might demonstrate
nail changes (onycholysis or subungualnail changes (onycholysis or subungual
hyperkeratosis).hyperkeratosis).

Other features : As sever systemic upset with highOther features : As sever systemic upset with high
fever , loss of weight .fever , loss of weight .
Pericarditis ,pleurisy & transient pulmonaryPericarditis ,pleurisy & transient pulmonary
infiltrate might occur.infiltrate might occur.
Myocarditis , heart block & aortic incompetence areMyocarditis , heart block & aortic incompetence are
very rare.very rare.

Investigations :Investigations :
ESR is elevated in acute phase , WBC may beESR is elevated in acute phase , WBC may be
high & mild normochromic normocytic anemiahigh & mild normochromic normocytic anemia
might present.might present.
HLAB27 is present in about 80% while serumHLAB27 is present in about 80% while serum
rheumatoid factor & ANA are absent.rheumatoid factor & ANA are absent.
Rdiological findings are : PeriaticularRdiological findings are : Periaticular
osteoporosis, reduction of joint space & erosionsosteoporosis, reduction of joint space & erosions
can be seen in prolonged or recurrent arthritis.can be seen in prolonged or recurrent arthritis.
Periosteitis might be seen. Sacroiliitis also couldPeriosteitis might be seen. Sacroiliitis also could
occur.occur.

Management:Management:
1.1. NSAIDs are useful for most of the patients.NSAIDs are useful for most of the patients.
2 .2 . Sulfasalzine ( 2__ 3 gms ) .Sulfasalzine ( 2__ 3 gms ) .
3.3. MTX or Azathioprine could be usedMTX or Azathioprine could be used
4.4. Uveitis is may be medical emergency requiringUveitis is may be medical emergency requiring
topical, subconjunctival or systemic steroid.topical, subconjunctival or systemic steroid.

5. Tetracycline is effective in treatment of5. Tetracycline is effective in treatment of
nonspecific urethritis.nonspecific urethritis.
6.The use of TNF inhibitor agents for patients with6.The use of TNF inhibitor agents for patients with
reactive arthritis and spondyloarthropathy isreactive arthritis and spondyloarthropathy is
similar to that in patients with rheumatoidsimilar to that in patients with rheumatoid
arthritis.arthritis.

Prognosis & course of RS is variedPrognosis & course of RS is varied
&unpredictable..&unpredictable..
Patients with AIDS may develop an aggressivePatients with AIDS may develop an aggressive
form of RS. The vast majority of AIDs patientsform of RS. The vast majority of AIDs patients
with RS are having HLAB27 antigen.with RS are having HLAB27 antigen.

Enteropathic Arthropathy.Enteropathic Arthropathy.
Enteropathic arthritis refers to the arthropathiesEnteropathic arthritis refers to the arthropathies
associated with bowel diseases ( usually Crhon’ sassociated with bowel diseases ( usually Crhon’ s
disease or Ulcerative colitis ).disease or Ulcerative colitis ).
These disorders are unified by clinical &These disorders are unified by clinical &
histological gut inflammationhistological gut inflammation
Alterd intestinal permeability & development ofAlterd intestinal permeability & development of
an inflammatory peripheral or axial arthritis .an inflammatory peripheral or axial arthritis .

Peripheral arthritis is observed in 20% & axialPeripheral arthritis is observed in 20% & axial
arthritis in 10__ 15% of patients .arthritis in 10__ 15% of patients .
Peripheral arthritis occur more frequently in thosePeripheral arthritis occur more frequently in those
with extraintestinal manifestations (-erythemawith extraintestinal manifestations (-erythema
nodosum )nodosum )
Males & females are equally affected .Males & females are equally affected .
All age groups are affected .All age groups are affected .

Disease onset features are low grade fever , painfulDisease onset features are low grade fever , painful
oral ulceration , ocular manifestations, cutaneousoral ulceration , ocular manifestations, cutaneous
manifestations ( erythema nodosum ) or enthesis .manifestations ( erythema nodosum ) or enthesis .
Peripheral arthritis manifests as inflammatory ,Peripheral arthritis manifests as inflammatory ,
non-erosive . asymmetrical mono or oligoarthritisnon-erosive . asymmetrical mono or oligoarthritis
affecting large joints ( knees, ankles, elbwsaffecting large joints ( knees, ankles, elbws
etc….).etc….).

Initially the arthritis may be migratory & mayInitially the arthritis may be migratory & may
resolve in weeks or months.resolve in weeks or months.
Controlling gut problem may prove beneficial orControlling gut problem may prove beneficial or
managing peripheral arthritis.managing peripheral arthritis.
Axial arthritis is clinically indistinguishable fromAxial arthritis is clinically indistinguishable from
AS. 50% of patients with axial skeletonAS. 50% of patients with axial skeleton
involvement having HLAB27.involvement having HLAB27.

Treatment.Treatment.
1.1. Control the underlying gut disease.Control the underlying gut disease.
2.2. NSAIDs.NSAIDs.
3.3. Aspiration & local steroid injection.Aspiration & local steroid injection.
4.4. Sulfasalazine.Sulfasalazine.

Behcet’ s SyndromBehcet’ s Syndrom
This vasculitis of unknown aetiology isThis vasculitis of unknown aetiology is
characteristically targets venuls. It is common incharacteristically targets venuls. It is common in
silk route countries , Mediterranean & Japan. Itsilk route countries , Mediterranean & Japan. It
an assoiation with HLAB5 & subtype 51.an assoiation with HLAB5 & subtype 51.

Clinical featuresClinical features
Oral aphthous ulceration( 93___ 100%)Oral aphthous ulceration( 93___ 100%)
Genital ulcers (69__ 100% )Genital ulcers (69__ 100% )
Occular symptoms ( 50___ 79%)Occular symptoms ( 50___ 79%)
Arthritis 35___50%),Arthritis 35___50%),
Skin lesions ( 35__65%)Skin lesions ( 35__65%)
CNS disease(10__30%)CNS disease(10__30%)
Major vessels occlusion/ aneurysm (10__37%) &Major vessels occlusion/ aneurysm (10__37%) &
constitutional symptoms 63%.constitutional symptoms 63%.

Recurrent oral ulceration:Recurrent oral ulceration:
Aphthous like stomatitis is initial manifestation inAphthous like stomatitis is initial manifestation in
25__75% of patients. Preferential sites are mucous25__75% of patients. Preferential sites are mucous
membrane of the lips, gingiva, check (buccalmembrane of the lips, gingiva, check (buccal
mucosa) & tounge. Ulcers are usually deep,mucosa) & tounge. Ulcers are usually deep,
multiple& painful & last for 10__30 days & healmultiple& painful & last for 10__30 days & heal
without scarring .without scarring .

Genital ulcers :Genital ulcers : Are similar to mouth ulcers occurAre similar to mouth ulcers occur
on genitalia( scrotum, vulva, penis, perianal&on genitalia( scrotum, vulva, penis, perianal&
vaginal mucosa). Lesions in male are morevaginal mucosa). Lesions in male are more
painful than in women , genital ulcers are usuallypainful than in women , genital ulcers are usually
deeper than oral ones & may leave scar afterdeeper than oral ones & may leave scar after
healing, vulvar ulcers often develop during thehealing, vulvar ulcers often develop during the
premenstrual stage.premenstrual stage.

Other features commonly occur include :Other features commonly occur include :
thrombophlebitis , erythema nodosum , pastulesthrombophlebitis , erythema nodosum , pastules
& folliculitis.& folliculitis.
The pustular reaction of the skin to intradermalThe pustular reaction of the skin to intradermal
skin prick ( some times referred as pathergy testskin prick ( some times referred as pathergy test
or called venepuncture) , this reaction occur inor called venepuncture) , this reaction occur in
70% 0f cases , usually occur in those with70% 0f cases , usually occur in those with
extensive disease, the test is nonspecific occuringextensive disease, the test is nonspecific occuring
in 7% of healthy control people.in 7% of healthy control people.

Arhritis occur in about 60% of cases is mono orArhritis occur in about 60% of cases is mono or
oligoarticular usually intermittent , self-limitedoligoarticular usually intermittent , self-limited
non erosive localized to knees & ankles & othernon erosive localized to knees & ankles & other
lower limb joints may be affected.lower limb joints may be affected.
The CNS can be involved withThe CNS can be involved with
meningoencephalitis , other manifestationsmeningoencephalitis , other manifestations
include seizure , cranial nerve palsies, bulbarinclude seizure , cranial nerve palsies, bulbar
palsy, ataxia, transient ischaemic attacks &palsy, ataxia, transient ischaemic attacks &
strokes.strokes.

Small & large ulcers in the gut produceSmall & large ulcers in the gut produce
symptoms of inflammatory bowel disease &symptoms of inflammatory bowel disease &
perforation might occur.perforation might occur.
The disease follows a course of relaps &The disease follows a course of relaps &
remissions.remissions.

Recurrent uveitis can be very sever & result inRecurrent uveitis can be very sever & result in
blindness& it is often bilateral.blindness& it is often bilateral.
uveitis, iritis &hypopyonuveitis, iritis &hypopyon

Diagnostic criteria of Behcet s disease :Diagnostic criteria of Behcet s disease :
Recurrent oral ulceration plus 2 of theRecurrent oral ulceration plus 2 of the
followings :followings :
1. Recurrent genital ulceration.1. Recurrent genital ulceration.
2. Eye lesions.2. Eye lesions.
3. Skin lesions.3. Skin lesions.
4. Pathergy test.4. Pathergy test.

Treatment:Treatment:
1.1. Oral & genital ulcers are treated symptomaticallyOral & genital ulcers are treated symptomatically
with local unaesthetic & steroid cream.with local unaesthetic & steroid cream.
2.2. Thrombosis of major vessels needs anticoagulantThrombosis of major vessels needs anticoagulant
therapy.therapy.
3.3. CNS involvement is an indication for high doseCNS involvement is an indication for high dose
of steroid.of steroid.
4.4. Colchicin or interferon—a can be beneficial forColchicin or interferon—a can be beneficial for
arthritis & mucocutneous lesions.arthritis & mucocutneous lesions.

5.5. Cyclosporin has shown promising in reducingCyclosporin has shown promising in reducing
ocular attacks.ocular attacks.
6.6. MTX is used.MTX is used.
7.7. TNF blckers are used.TNF blckers are used.
8.8. Arhritis tends to be the least troublesome of theArhritis tends to be the least troublesome of the
complications , it is self-limiting & responds wellcomplications , it is self-limiting & responds well
to NSAIDs &/ or intraarticular steroid.to NSAIDs &/ or intraarticular steroid.

Crystal induced ArthropathyCrystal induced Arthropathy
The crystal arthropathies include gout , calciumThe crystal arthropathies include gout , calcium
pyrophosphate deposition disease (CPPD) orpyrophosphate deposition disease (CPPD) or
pseudogut , basic calcium phosphate syndromes ,pseudogut , basic calcium phosphate syndromes ,
& calcium oxalate arthritis& calcium oxalate arthritis

GOUTGOUT
Gout is a systemic disease resulting fromGout is a systemic disease resulting from
abnormality of serum uric acid metabolism ,abnormality of serum uric acid metabolism ,
characterized by hyperuicemia & uric acid crystalcharacterized by hyperuicemia & uric acid crystal
deposition in joints causing acute gouty arthritis,deposition in joints causing acute gouty arthritis,
in soft tissue causing tophi & tenosynovitis & inin soft tissue causing tophi & tenosynovitis & in
the urinary tract causing urate stones.the urinary tract causing urate stones.

Chronic hyperuricemia is necessary for theChronic hyperuricemia is necessary for the
development of gout ( serum uric acid more thandevelopment of gout ( serum uric acid more than
7.0 mg/dl in males & 6.0 mg/dl in females) .7.0 mg/dl in males & 6.0 mg/dl in females) .
Urat deposition in the synovial membrane leads toUrat deposition in the synovial membrane leads to
an intense & often destructive arthritisan intense & often destructive arthritis

Gout occurs mainly in developed countries in USAGout occurs mainly in developed countries in USA
the prevalence is 13.6/1000 in adult males &the prevalence is 13.6/1000 in adult males &
6.4/1000 in females, while the prevalence of6.4/1000 in females, while the prevalence of
hyperuricemia is about 5% .hyperuricemia is about 5% .
At puberty male serum uric acid level rise & remainAt puberty male serum uric acid level rise & remain
higher than those for female until menopause.higher than those for female until menopause.
Gout is very uncommon before puberty.Gout is very uncommon before puberty.

Serum uric concentrations are related to severalSerum uric concentrations are related to several
demographic factors ( age , gender , body bulk ,demographic factors ( age , gender , body bulk ,
life style, economic state & genetic constitution).life style, economic state & genetic constitution).
It is higher in the urban than in rural communitiesIt is higher in the urban than in rural communities
& correlates positively with social class, weight && correlates positively with social class, weight &
high protein diet.high protein diet.

Uric acid production & elimination.Uric acid production & elimination.
The serum urate level depends on the production &The serum urate level depends on the production &
its disposal. The majority of urate is produced byits disposal. The majority of urate is produced by
hepatic xanthin oxidase acting on hypoxanthin &hepatic xanthin oxidase acting on hypoxanthin &
xanthin, derived by degredation of neucleic acidxanthin, derived by degredation of neucleic acid
of senescent cells& from the metabolic turnoverof senescent cells& from the metabolic turnover
of cellular purin neucleotides .of cellular purin neucleotides .
Less than 10% of uric acid comes from performedLess than 10% of uric acid comes from performed
dietary nucleotides & nucleosides , about 60% ofdietary nucleotides & nucleosides , about 60% of
uric acid is replaced daily by constant turnover,uric acid is replaced daily by constant turnover,
the quantity produced is proportional to the bodythe quantity produced is proportional to the body
size.size.

The uric acid is complety filtered by the glomerulusThe uric acid is complety filtered by the glomerulus
100% is then reabsorbed in the proximal tubules100% is then reabsorbed in the proximal tubules
&then 75% is secreted by distal tubules some&then 75% is secreted by distal tubules some
postreabsorption also takes place.postreabsorption also takes place.
The kidneys dispose 2/3 of uric acid and theThe kidneys dispose 2/3 of uric acid and the
remainder is filtered in the gut luman, where partremainder is filtered in the gut luman, where part
of it degraded by bacteria in the gut, thisof it degraded by bacteria in the gut, this
increases substantially in renal insufficiency .increases substantially in renal insufficiency .

Pathogenesis.Pathogenesis.
The biochemical abnormality is hyperuricemiaThe biochemical abnormality is hyperuricemia
resulting from overproduction or underexcretionresulting from overproduction or underexcretion
of uric acid . A high dietary intake of purines canof uric acid . A high dietary intake of purines can
be an additional factor but doesnot in itselfbe an additional factor but doesnot in itself
produce hyperuricemiaproduce hyperuricemia
Causes of hyperuricemia.Causes of hyperuricemia.
Genetic, diet , diseases ( MyeloproliferatiiveGenetic, diet , diseases ( Myeloproliferatiive
disease, on chemotherapy,),& drugs decreasedisease, on chemotherapy,),& drugs decrease
renal elimination of uric acid i.e aspirin in lowrenal elimination of uric acid i.e aspirin in low
doses.doses.

Prolonged hyperuricemia causes the formation ofProlonged hyperuricemia causes the formation of
small crystal aggregates , these crystalssmall crystal aggregates , these crystals
accumulates in the synovium & at variousaccumulates in the synovium & at various
external sites such as the ear cartilage &external sites such as the ear cartilage &
olecranon sites , & may eventually expand &olecranon sites , & may eventually expand &
become visible tophi.become visible tophi.
Crystal deposition may proceed over years withoutCrystal deposition may proceed over years without
symptoms. Disturbance in homoeostasis lead tosymptoms. Disturbance in homoeostasis lead to
shedding of crystals in to the joint cavity fromshedding of crystals in to the joint cavity from
synovial microtophi , if enough free intraarticularsynovial microtophi , if enough free intraarticular
crystals are present they will produce an acutecrystals are present they will produce an acute
inflammatory response.inflammatory response.

Clinical features.Clinical features.
The peak age of onset is about 45 y.in men whileThe peak age of onset is about 45 y.in men while
in predisposed women it occurs some years afterin predisposed women it occurs some years after
menopause.menopause.
Gout classically occurs in obese middle or youngGout classically occurs in obese middle or young
men who drinks more alcohol than average.men who drinks more alcohol than average.
The patient wakes early hours in the morning withThe patient wakes early hours in the morning with
sever agonizing pain usually in thesever agonizing pain usually in the

metatarsophalangeal joint of the big toe ( the jointmetatarsophalangeal joint of the big toe ( the joint
is usually red, swollen, warm & tender).Theis usually red, swollen, warm & tender).The
overlying skin is shinny with periarticular edema,overlying skin is shinny with periarticular edema,
& there is often fever.& there is often fever.
75% of the first attack is monoarticular, at half75% of the first attack is monoarticular, at half
involve metatarsphalageal joint of big toe.involve metatarsphalageal joint of big toe.
Attack lasts days or weeks befor subsidingAttack lasts days or weeks befor subsiding
spontaneously . Patient might have one attack orspontaneously . Patient might have one attack or
may have reccurences at monthly or yearlymay have reccurences at monthly or yearly
intervals.intervals.

Reccurent attacks may merge in to each other. NoReccurent attacks may merge in to each other. No
synovial joint is immune from gout . Boneysynovial joint is immune from gout . Boney
erosion & joint destruction might occur & lead toerosion & joint destruction might occur & lead to
disability.disability.
Acute gout could occur in nonarticular sites i.eAcute gout could occur in nonarticular sites i.e
olecranon bursa , achillis tendon & prepatellarolecranon bursa , achillis tendon & prepatellar
bursa.bursa.

Tophi.Tophi.
A tophus is a deposite of fine needle ( msu)A tophus is a deposite of fine needle ( msu)
surrounded by grnuloma & giant cells. They aresurrounded by grnuloma & giant cells. They are
found in the articular cartilage,ear cartilage,found in the articular cartilage,ear cartilage,
synovium, tendon sheath, bursae & othersynovium, tendon sheath, bursae & other
periarticular structure..Patient possessing tophi isperiarticular structure..Patient possessing tophi is
said having chronic tophaceous gout either or notsaid having chronic tophaceous gout either or not
experiencing episodes of acute gouty arthritis.experiencing episodes of acute gouty arthritis.
Presence of tophi is an indication for long termPresence of tophi is an indication for long term
treatment to lower the serum uric acid.treatment to lower the serum uric acid.
Renal calculiRenal calculi
is present in 10% of gout & renal nephropathyis present in 10% of gout & renal nephropathy
might be found on autopsy.might be found on autopsy.

Large tophus of the knee in patient with chronicLarge tophus of the knee in patient with chronic
uncontrolled gout.uncontrolled gout.

Three inflamed tophi over the proximal interphalangealThree inflamed tophi over the proximal interphalangeal
joints in a patient with chronic tophaceous gout. Severaljoints in a patient with chronic tophaceous gout. Several
of the lesions ruptured spontaneously over the next threeof the lesions ruptured spontaneously over the next three
days, exuding a pasty material composed of uratedays, exuding a pasty material composed of urate
crystals and inflammatory cells but no organisms.crystals and inflammatory cells but no organisms.

Dfferential diagnosis.Dfferential diagnosis.
 PseudogoutPseudogout
 Acute rheumatic feverAcute rheumatic fever
 RARA
 Pyogenic arthritisPyogenic arthritis
 CellulitesCellulites
 Bursitis,Bursitis,
 TendonitisTendonitis
 Thrombophelibitis.Thrombophelibitis.

Investigation .Investigation .
 ESR is elevated in acuter attack .ESR is elevated in acuter attack .
 Serum uric acid could be high but it is notSerum uric acid could be high but it is not
necessary to be so & high serum uric acid alonenecessary to be so & high serum uric acid alone
doesn’t justify the diagnosis of gout.doesn’t justify the diagnosis of gout.
 In acute gout the presence of long needleIn acute gout the presence of long needle
shaped negatively birefringent nmonosodiumshaped negatively birefringent nmonosodium
crystals in the synovial fluid is diagnostic.crystals in the synovial fluid is diagnostic.
 X- ray shows punched out area , jointX- ray shows punched out area , joint
destruction & might be ankylosis.]destruction & might be ankylosis.]

Plain radiograph of the hand demonstrating soft tissuePlain radiograph of the hand demonstrating soft tissue
calcifications adjacent to interphalangeal joints and atcalcifications adjacent to interphalangeal joints and at
the base of the thumb (arrows). These findings representthe base of the thumb (arrows). These findings represent
calcification within gouty tophi.calcification within gouty tophi.

Plain radiograph of the foot demonstrating featuresPlain radiograph of the foot demonstrating features
consistent with gout. There is soft tissue swellingconsistent with gout. There is soft tissue swelling
and extensive erosions involving the firstand extensive erosions involving the first
metatarsophalangeal joint, as well asmetatarsophalangeal joint, as well as
calcifications within a tophus.calcifications within a tophus.

Management.Management.
The aims are to reduce acute synovitis , preventThe aims are to reduce acute synovitis , prevent
further crystal formation & identify associatedfurther crystal formation & identify associated
disease.disease.
In acute attack :In acute attack :
1.1. NSAID ( often indomethacine )NSAID ( often indomethacine )
2.2. Oral colchicine.Oral colchicine.
3.3. I.V colchicine.I.V colchicine.
4.4. Itraarticular corticosteroids.Itraarticular corticosteroids.
5.5. Oral corticosteroid.Oral corticosteroid.

Azapropazone ( 600 twice a day ) is both antiinflamatory &Azapropazone ( 600 twice a day ) is both antiinflamatory &
uricosuric agent.uricosuric agent.
When long term treatment is necessary xanthine oxidaseWhen long term treatment is necessary xanthine oxidase
inhibitor ( allopurinol ) or uricosuric drugs are startedinhibitor ( allopurinol ) or uricosuric drugs are started
after several weeks from controlling the acute attack.after several weeks from controlling the acute attack.
Indications for long term therapy include :Indications for long term therapy include :
1.1. Reccurent attacksReccurent attacks
2.2. Tophaceous goutTophaceous gout
3.3. Renal calculi.Renal calculi.
Uricosuric drugsUricosuric drugs inhibit renal tubular reabsorption of uricinhibit renal tubular reabsorption of uric
acid, ( Probenecid, Sulphinpyrazone & Salicylate in highacid, ( Probenecid, Sulphinpyrazone & Salicylate in high
doses). They are ineffective in renal failure.doses). They are ineffective in renal failure.

Medicine 5th year, all lectures/rheumatology (Dr. Rauf)

Medicine 5th year, all lectures/rheumatology (Dr. Rauf)

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