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Rheumatoid DisordeAgus Widiyatmoko
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The Algoritme
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Musculoskeletal problems?
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Articular or non articular?
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Acute (< 6 weeks
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!hronic non in#ammatory arthr
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!hronic $n#ammatory Arthritis
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!hronic $n#ammatory %oliarthritare Asymmetric
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Acute Arthritis$' arthritis symptoms < 6 weeks
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out Arthritis
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out
•
!aused by deposition o' monosodium urate crysaround and in the tissues o' the )oint
• Three distinct stages*• aasymptomatic hyperuricemia+
• bacute intermittent gout+
•cchronic tophaceous gout
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Risk ,actors 'or out
• Underexcretors (80%)• Male gender
• Postmenopausal females• Obesity, metabolic synd.• t!anol• "enal insufficiency• Plumbism• Medications (see separate)•
#e!ydration$lo flo• &ilipino ancestry• &ructose ingestion• Uromodulin 'idney dis.
•
Overproducers (20%)• Ethanol
• High cell turnover states(psoriasis, myeloprolif. disorde
• Excessive purine ingestion
• ! overactivity (x"lin#ed)
• H$! underactivity (x"lin#ed
• &eta aldolase deficiency• 'arcoidosis
• &2 deficiency
• o*n syndrome
• $lycogen storage dis. +, , -
• ever, post"op state
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Risk ,actors 'or out
• Obesity, metabolic syndrom• t!anol
• #iuretics
•
&ructose ingestion• xcessie purine ingestion
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./erproducers
• +-/0% of gouty patients areoerproducers.
• #istinguis!ed by / !our uric acid
excretion1 – 2 800 mg$d on regular diet.
– 2 300 mg$d on purinefree diet.
D A i t d ith
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Drugs Associated with-yperuricemia
• #iuretics (loop and
t!ia4ide types)• 5odose aspirin• 6yclosporine,
tacrolimus• t!anol• t!ambutol
• Pyra4inamide• "itonair, darunair,
didanosine• 5eodopa
• /icotinic acid, niac
• ancreatic enymes
• !ituxima1
• &asilixima1
• eriparatide
• ilgrastim
• 'ildenafil
• iaoxide
• ytotoxicchemotherapy
D A i t d ith
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Drugs Associated with-yperuricemia
• #iuretics (loop and
t!ia4ide types)• 5odose aspirin• 6yclosporine,
tacrolimus• t!anol• t!ambutol
• Pyra4inamide• "itonair, darunair,
didanosine• 5eodopa
• /icotinic acid, niac
• ancreatic enymes
• !ituxima1
• &asilixima1
• eriparatide
• ilgrastim
• 'ildenafil
• iaoxide
• ytotoxicchemotherapy
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-yperuricemia 0 ou
7erum Uric cid(mg$dl) nnual ncidencof 9out (%)
: ;.0 0.+
;.0 < 8.= 0.-
2 =.0 .=
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-yperuricemia and o
• >yperuricemia (2;.0 mg$dl) in -% 8% of mpopulation.• Most (about ?) are foreer asymptomatic• 80% of gouty patients !ae uric acid : = m• boe +0 mg$dl, ris' rises rapidly.
• 9out is t!e most common cause of monamiddleaged and elderly men (8% yearly p
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Who Almost 1e/er ets
• Prepubertal c!ildren• Premenopausal omen
• 5oo' for en4yme defects in t!ese pa
• 5oo' for familial 'idney disease
%ro/ocati/e ,actors
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%ro/ocati/e ,actors“ Adding Insult to Injury
• t!anol• 6essation of
et!anol
• Purineoerindulgence
• 7urgery
• *rauma
• Overexercise
• asting
• ever
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The ,ructose !onnect
• &ructose raises uric acid leels in m• iggest source of fructose1 !ig! fruc
corn syrup.
• 7ucrose does not seem to raise uric
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2ink to !ardio/ascular D
• n experimental models, !yperuricemcauses1 – >ypertension – "educed perfusion – ndot!elial dysfunction
– "enal dysfunction
• "eersible it! !ypouricemics
,re4uent !linical Associa
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,re4uent !linical Associawith out
• >ypertension• #iabetes
• >yperlipidemia
• Obesity
• t!anol < t!e fuel
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out 0 5idney Diseas
• 7tones Uric acid and calcium• Urate nep!ropat!y c!ronic interstit
disease, not ell defined.
• Uric acid nep!ropat!y < acute tubula
deposition of uric acid, it! renal faseen in gout.
romodulin associated kid
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romodulin7associated kiddisease
AKA:• &amilial medullary cystic 'idney dise
/.
• &amilial @uenile !yperuricemic nep!
• Uromodulin storage disease.
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romodulin (cont8d
• Uromodulin (*amm>orsfall protein)accumulates in t!e t!ic' ascending 5oop of >enle.
• "educed excretion of uric acid.
• Ao renal deposition of urates.• utosomal dominant.
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A Typical Attack o' o
• 5asts seeral days to seeral ee'
• May spread from @oint to @oint.
• Often accompanied by feer,leu'ocytosis.
• 9ets orse as t!e years go on.
• Pain appears last, disappears first
• Petite attac's occur (lasting !ours
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!auses o' %odagra
• M7U• 6PP#
• >ydroxyapatite
• 7eptic
• Psoriatic, "eiterBs• "!eumatoid
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Radiographic -allmarks o
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Radiographic -allmarks o
•Oer!anging edges
• Punc!ed out lesions it! sclerotic b
• Preseration of @oint space (till late)
• #egeneratie c!anges
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The Three %hases o'
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Treatment
• *reat acute attac'
• Preent ne attac's
• "educe uric acid leel(sometimes)
%hase 9 Terminatio
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%hase 9 7 Terminatio
•
A7#• 6olc!cine
• ntraarticular steroids
• 7ystemic steroids
• 5+ in!ibitors
1&A$Ds
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1&A$Ds
•
*reatment of c!oice inot!erise !ealt!y patient.
• oid in renal insufficiencyand in peptic ulcer disease.
•
oid salicylates (t!ese caussings in serum uric acid).
$ntra7Articular &teroid
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$ntra7Articular &teroid
•
One or a fe @oints.• Aot useful for polyarticular o
softtissue gout.
• Ma'e sure infection not
present.
.ral !olchicine
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.ral !olchicine
•
+./ mg folloed by 0.3 mg / !rs late• Loading dose same in renal insuffici
• Maintenance (preentie) dose 0.3 mbid.
•0.D mg /D times per ee' in dialysis(preentie).
&ystemic &teroids
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&ystemic &teroids
•
Polyarticular attac's or feer.• 5ongstanding attac's (2D- days).
• Aeed diided doses.
• *aper oer ;+0 days.
• 7tart prop!ylactic agent (colc!icine)as possible.
Anakinra (.:72abel
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Anakinra (.: 2abel
• ffectie for acute attac' in
studies.• est in pts !o cannot ta'esteroids or colc!cine.
• xpensie but + ee' oftreatment may be affordable.
• Aot for preentie use.• Ot!er interleu'in+ in!ibitors
currently in trials (rilonacept Ecana'inumab)
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%hase ; 7 %re/enti/e The
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%hase ; %re/enti/e The
•
6olc!icine or A7#.• lays use !en beginning a !ypou
drug.
• 6ontinue seeral ee's to years (deon top!i, serum uric acid).
• lays use before surgery in preiogouty patient.
%hase 7 -ypouricemic Th
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%hase -ypouricemic Th
•
Aot eery patient needs it.• May not need it in1 – Fery elderly
– Aoncompliant
– nfreCuent attac's and no top!i
• May exacerbate attac's early on
oals o' -ypouricemT t t
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Treatment
•
im for serum uric acid under 3, prenear - for some c!ronic gouty patien
• ut remember1 – allopurinol toxicity more li'ely it! !ig
– More li'ely it! renal insufficiency.
-ypouricemic Agent
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-ypouricemic Agent
•
llopurinol• &ebuxostat
• Probenecid
• Pegloticase
• 5osartan (offlabel)• >ig!dose salicylates (offlabel)
• Fitamin 6 (offlabel)
-ypouricemic Therap
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ypou ce c e ap
•
#onBt start !ypouricemic agent durinattac'.
• Use probenecid firstG itBs safer.
• #onBt use probenecid if1 – oerproducer
– creat clearance : D--0 ml$min.
– !istory of 'idney stones.
Reasons 'or -ypouricemTreatment ,ailure
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Treatment ,ailure
• Aeed loer uric acid leels t!an Hno
• Aoncompliance.
• "enal insufficiency.
• "apid dissolution of top!i.•
"apid elimination of oxypurinol (mayit! combined allopurinol and probe
Asymptomatic -yperuric
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y p yp
• #onBt treat it (t!is adice may c!angfuture)
• xception1 Patients getting c!emot!leu'emia, lymp!oma.
Ma)or To=icities o'
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Allopurinol• ncreased gout attac's early on (use
prop!ylaxis)
• "as! (may be seere)
• 7teensJo!nson syndrome
• Fasculitis
•>epatitis
• "enal failure (interstitial nep!ritis)
• one marro suppression
Allopurinol -ypersensiti/it&yndrome
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&yndrome
• &eer
• "as!
• "enal &ailure
• Hepatic in3ury• 4eu#ocytosis
• Eosinophilia (the
tipoff5)
• May be fatal. >ard to treat.• 7erious reactions to allopurinol reported
in + of /30 patients. 6rthritis !heum 27892, 79:
Treatment o' &tonesin outy %atients
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in outy %atients
• llopurinol – calcium and uric acid
stones
• Potassium citrate – calcium and uric acid
stones – direct in!ibitor of
nucleation
• &luidsK
Treatment o' &tonesin outy %atients
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in outy %atients
• llopurinol – calcium and uric acid stones
• Potassium citrate – calcium and uric acid stones
– direct in!ibitor of nucleation
• &luidsK
,ebu=ostat
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• Aonxant!ine in!ibitor of LO and L
• etter tolerated t!an allopurinol.
• 5oer uric acid leels t!an allopur(-D% s. /+% met target of 3.0 mg$
• etter dissolution of top!i.
,ebu=ostat* >est se
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• llopurinol failures
• "enal insufficiency
• *op!aceous gout
Allopurinol 0 ,ebu=ostat D$nteractions
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$nteractions
• 5ife t!reatening interaction it!a4at!ioprine, 3mercaptopurine – "educe dose of purine analogue b
approximately /$D.
• *!eop!ylline
• Ot!er interactions also
%egloticase
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• &or refractory c!ronicgout
• #issoles top!i in ee'sto mont!s
• Problems1
– nap!ylaxis – ntibody formation – Aot in 93P# defic. –
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This is chronic
refractory
gout!
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2osartan 0 it ! (.:72abel
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2abel• 5oers uric acid 0.D < +.D mg$dl (dos
range /- < /00 mg$d).
• Uricosuric mec!anism.• Useful !en / !our uric acid is : 8
mg$d.• Maintain good !ydration.• ffect is not seen it! ot!er "s.• lso consider fenofibrate (Cuite goo
actually) and atorastatin (bot! offlabel).
• #onBt forget itamin 6 (-00 mg #)
&yno/ial ,luid in ou
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• May be cloudy or clear.
• nspect for top!aceous deposits.
• N6 < /000 < -0,000 or more
• 9lucose normal.
•
eteen attac's, may !ae free crys• #onBt forget to culture it.
%&@D..T
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• 6alcium pyrop!osp!ate 6rystal #ep#isease (6PP#) is t!e syndrome secto t!e calcium pyrop!osp!ate in artitissues.
• *!is includes1 6!ondrocalcinosis, 6
6PP# and Pseudogout.
%seudogout
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• tiology1 t is un'non, but can be sto c!anges in t!e cartilage matrix orsecondary to eleated leels of calciinorganic pyrop!osp!ate.
• Pat!ology1 6PP# crystals are found
@oint capsule and fibrocartilaginousstructures. *!ere is neutrop!il infiltand erosions.
%seudogout
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• #emograp!ics1 t is predominantly aof t!e elderly, pea' age 3- to ;- year!as female predominance (&1M, /;1+
• Prealence of c!ondrocalcinosis is -t!e general population.
%seudogout
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• #isease ssociations1 !ypert!yroid!ypocalciuria, !ypercalcemia,!emoc!romatosis, !emosiderosis,!ypop!osp!atasia, !ypomagnesemi!ypot!yroidsm, gout, neuropat!ic @o
amyloidosis, trauma and O.
%seudogout
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• 6linical Manifestations
• Pseudogout1 Usually presents it! selflimited attac's resembling acute*!e 'nee is inoled in -0% of t!e cafolloed by t!e rist, s!oulder, an'l
elbo.
%seudogout
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• n -% of patients gout can coexist
pseudogout.
• *!e diagnosis is confirmed it! t!e fluid analysis and$or t!e presence ofc!ondrocalcinosis in t!e radiograp!
• cute Pseudogout primarily affects
%seudogout
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• 6!ronic 6PP#1 predominately affect
it is a progressie, often symmetric,polyart!ritis.
• Usually affects t!e 'nees, rists, /nM6PBs, !ips, spine, s!oulders, elbo
an'les.• 6!ronic 6PP# differs from pseudog
c!ronicity, inolement of t!e spine M6PBs.
%seudogout
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• 6!ondrocalcinosis1 9enerally is an i
finding in L"ays.
• #iagnostic *ests1 nflammatory cell t!e synoial fluid. "!omboidal or rointracellular crystals. maging studi
c!ondrocalcinosis usually in t!e 'necan be seen in t!e radial @oint, symppubis and interertebral discs.
%seudogout
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• #ifferential #iagnosis1 ncludes sept
art!ritis, gout, inflammatory O, "!ert!ritis, neuropat!ic art!ritis and >Osteoart!ropat!y.
%seudogout
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• *!erapy1 t is similar to gout and inc
intrarticular corticosteroids. 6olc!icbe used in acute attac's and also inprop!ylaxis. *!ere is no specific trefor c!ronic 6PP#. t is important to t
secondary causes and colc!icine co!elpful.
Treatment o' Acute %sued
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• spiration (more important
t!an in goutK)• "est
• ntraarticular steroids
• A7#s
• 7ystemic steroids
• 6olc!icine
• 5+ n!ibitors
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!hronic Arthritis" 6 weeks
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!hronic 1on $n#ammatArthritis
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OSTEOARTHRITIS
OSTEOARTHROSIS
DEGENERATIVE JOINT DISEASE
D@,$1$T$.1
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Osteoarthritis OA is a degenerative
disease o' diarthrodial (synovial joints characteriBed by Breakdon o' articular cartilage
and !roli"erative changes o'surrounding bones
@%$D@M$.2.C
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.steoarthritis(.A is the #ost $o##o )oint disease
.A o' the knee )oint is 'ound in %&' o'the population o/er 6 years o' age
Radiological e/idence o' .A can be'ound in o/er E F o' the population
2$M$T@D ,1!T$.1
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.A may cause 'unctional loss
Acti/ites o' daily li/ing Most important cause o' disa(ility in
old age
Ma)or indication 'or )oint replacementsurgery
!-ARA!T@R$&T$!& ., .A
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.A is a $hroni$ disease o' themusculoskeletal system itho)tsyste#i$ in/ol/ement
.A is mainly a nonin*a##atorydisease o' syno/ial )oints
1o )oint ankylosis is obser/ed in the
course o' the disease
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AGE
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%rimary .A , -& years
Direct correlation
Aging process
R$&5 ,A!T.R& ,.R %R$MARC .A
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Age
&e=
.besity
enetics
Trauma (daily
&@!.1DARC .&T.ART-R$T$&
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Tra)#a %re/ious )oint disorders+ !ongenital hip dislocation $n'ection* &eptic arthritis >rucella Tb $n#ammatory* RA A& Metabolic* out
-ematologic* -emophilia @ndocrine* DM
ETIO.OG/ O0 OA
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!artilage properties
>iomechanical problem
%rimary eneraliBed .A
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&TR!TR@ ., G.$1T!ART$2A@
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1ollagen (Type ; +roteogly$an
7 -yaluronic acid
7 lycoseaminoglycan
Water 1ondro$yte
Regeneration and Degeneration
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%AT-.2.C ., .A
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,ibrillation
@burnation
.steophytes
&ubcondral cysts
@T$.%AT-.@1@&$& ., .A
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Agegender
2ocal
enetic .A biochemicae:ects
.ther 'actors
@T$.%AT-.@1@&$& ., .A
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Dys'unction o' )oint cartilage
!ondrocyte 'unction* 97 Degredati/eenBymes
(metalloproteases
;7 $nhibitors Degeneration and regeneration 'unction
are balanced
$279 ↑ degredati/e enBymes↑ H syno/iain#ammation results* >reakdown o'
%AT-.@1@&$& ., .A
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!ytokines $279 $276 T1,7α
!ell destruction
Membrane phospholipids
Arachidonic acid
!o=79 !o=7;
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$279 and #etallo!roteases ha/ebeen 'ound to play an important role in$artilage destr)$tion3
2ocal growth 'actors especiallytrans'orming growth 'actor (T, are
in/ol/ed in the 'ormation o'osteo!hytes
2A>.RAT.RC ,$1D$1& ., .A
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There are no pathognomoniclaboratory Indings 'or .A
2aboratory analysis is per'ormed 'or
di2erential diagnosis
RAD$.2.$! ,$1D$1& ., .A
1arro ing o' )oint space (due to loss o'
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1arrowing o' )oint space (due to loss o'cartilage
Osteo!hytes
&ubchondral (paraarticular sclerosis
>one cysts
RAD$.2.$! RAD@ ., .A
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9 1ormal ; Mild
Moderate
J &e/ere
5ellgren 2awrence !lassiIcation
DIAGNOSIS O0 OA
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1.INI1A. 0INDINGS
Goint pain H
RADIO.OGI1 0INDINGS
.steophytes
1.INI1 O0 OA SIGNS ANDS/3+TO3S
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Goint pain 7 degenerati/e
&ti:ness 'ollowing inacti/ity K min
2imitation o' R.M K later stages
De'ormity K restricition o' AD2
OA O0 4NEE JOINT 5GONARTHROS
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More common in obese 'emales
o/er L years o' age Goint sti:ness (< minutes Mechanical pain %hysical e=amination Indings* !repitus %ain on pressure %ain'ul R.M and 'unctional limitation 2imitation o' R.M in later stages o' .A (Irst
e=tension 2aboratory analysis within normal limits
@1 A2& 7 .RT-.&$&
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RADIO.OGI1 0INDINGS7 GRADE8 9 -7
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.A ., -$% G.$1T
More common in #ales over -& years
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More common in #ales over -& yearso' age
Goint sti:ness %ain o' hip gluteal and groin areas
radiating to the knee (1 obturatorius
Mechanical pain
2imited walking 'unction
!.ART-R.&$&
+hysi$al e:a#ination*
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y
Antalgic limping
2imitation o' R.M (Irst internal rotation
%ain'ul R.M
Trendelenburg test positi/ity
2eg length discrepancy
2aboratory analysis within normal limits
>$.M@!-A1$!&
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7RAC ., -$% .A
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%eripheral Goints -ands
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,eet
TR@ATM@1T ., .A
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&ymptomatic treatment
&tructure modi'ying treatment
&urgical treatment
&TR!TR@ M.D$,C$1 TR@ATM@1T
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-yaluronic acid in)ection (-A
lycose amino glycans (A
%R$MARC %R@@1T$.1 ., .A ??
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Regular e=ercises
Weight control
%re/ention o' trauma
A$M& ., .A TR@ATM@1T
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%ain relie'
%reser/ation and restoration o' )oint'unction
@ducation
1on7%harmacologic Treatment o'.A
%atient education
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%atient education Weight loss (i' o/erweight
Aerobic e=ercise programs %hysical therapy Range7o'7motion e=ercises
Muscle7strengthening e=ercises Assisti/e de/ices 'or ambulation
%atellar tapingAppropriate 'ootwear
2ateral7wedged insoles ('or genu /arum >racing .ccupational therapy Goint protection and energy conser/ation
%-ARMA!.2.$! TR@ATM@1T ., .A
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.ral &ystemic Medical Agents
7 Analgesics (acetaminophen
7 1&A$Ds
7 .pioid analgesics
$ntraarticular agents*
-yaluronan
lucocorticoids (e:usion
Topical agents
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HAND OA 9 RESTING S+.INT
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S/3+TO3ATI1 TREAT3ENT O0 OA
De$rease o" joint loading
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j g
7 ;eight $ontrol
7 &plinting
7 Walking sticks
E:er$ises
7 &wimming
7 Walking
7 &trengthening
+atient ed)$ation
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$1A&$@ [email protected]&
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Goint la/age
Arthroscopy
!artilage gre'ting7 genetic engineering
&urgery
.steotomy
Goint replacement
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!hronic $n#ammatoryArthritis
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Rheumatoid Artritis
Rheumatoid Arthritis
DeInition
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Multisystem Autoimmune$n#ammatory !ondition
&ymmetrical%olyarthropathy&mall )oints
@pidemiology
$t can de/elop at any age but typicallystarts between J7 6 years
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starts between J 6 years
,emale*Male (*9
!ommon Arthritis* 9 in 9 de/elop RA
at some stage in their li'e
%athophysiology
1ot completelyelucidatedN
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Autoimmune Trigger &yno/ial cell
hyperplasia andendothelial cell acti/ation
uncontrolledin#ammation bonedestruction
enetics
&ymptoms and &igns
Morning sti:ness lasting O9 hourP
&welling in O )ointsP
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&welling in O )oints
&welling in hand )ointsP &ymmetric )oint swellingP
@rosions or declaciIcations on =ray o'hand
Rhematoid nodules Abnormal serum R,PMust be present O6 weeks
Rheumatoid Arthritis A person shall be said
to have rheumatoidarthritis if he or she has
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satisfied 4 of 7 criteria,
with criteria 1-4present for at least 6weeks
@=tra7articularmani'estations
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Functional Presentation andDisability of RA In the initial stages of each joint involvement, th
warmth, pain, and redness, with corresponding d
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p p g
of range of motion of the affected joint
rogression of the disease results in reducible anfi!ed deformities
"uscle weakness and atroph# develop earl# in thof the disease in man# people
$n/estigations
>loods ,>! 0@s 2,Ts @&R !R% R, anti !!%
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$maging
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Complications of Rheumatoid Arthritis
$omplications include% $arpal tunnel s#ndrome, &aker's c#st, vasculitis, subcu
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p # , # , ,nodules, (j)gren's s#ndrome, peripheral neuropath#, cpulmonar# involvement, *elt#'s s#ndrome, and anemia
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DMARD&
[email protected]@AT@ (Irst line7 oral ulcersalopecia $ upset hepatoto=ic
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&2,A&A2AQ$1@7 $ upset lesshepatoto=ic
2@,21.M$D@7 2i/er cirrhosis $ upsetalopecia
N.2D7 Rash lomerulonephropathy
N%@1$!$22$AM$1@7 Rash lupus7like illnes
Treatment (urger#%
+emoval ofi fl d i
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inflamed s#noviumArthroplast#
h#sical therap#
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Vocational Implications ofRheumatoid Arthritis "ost jobs reuiring medium to heav# lifting are not desir
Acti ities s ch as climbing balancing stooping kneeling
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Activities such as climbing, balancing, stooping, kneeling
or walking are hampered
/!tremes of weather or abrupt changes in temperature savoided 0 indoor controlled climate better
Lupus Systemic lupus
erythematosus also calledSLE , or lupus2 is anautoimmune disease of the
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bod#3s connective tissues
Autoimmune means that theimmune s#stem attacks thetissues of the bod# In (5/,the immune s#stem primaril#attacks parts of the cellnucleus
(5/ affects tissues throughout
the bod# *ive times as man#women as men get (5/ "ostpeople develop the diseasebetween the ages of 1 and4, although it can show upat an# age
Lupus - Anatomy (5/ causes tissue
inflammation and blood vesselproblems prett# muchan#where in the bod# (5/particularl# affects the
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particularl# affects the
kidne#s 8he tissues of thekidne#s, including the bloodvessels and the surroundingmembrane, become inflamed swollen2, and deposits ofchemicals produced b# thebod# form in the kidne#s8hese changes make itimpossible for the kidne#s tofunction normall#
ote the granular appearanceof the corte! of these lupusaffected kidne#s 0 it's acrossthe entire surface of bothkidne#s suggesting a chroniccondition
Lupus Anatomy (cont! 8he inflammation of (5/ can be seen in the
lining, covering, and muscles of the heart8he heart can be affected even if #ou arenot feeling an# heart s#mptoms 8he mostcommon problem is bumps and swelling ofth d di hi h i th li i
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the endocardium, which is the lining
membrane of the heart chambers andvalves (5/ also causes inflammation and
breakdown in the skin +ashes can appearan#where, but the most common spot isacross the cheeks and nose
eople with (5/ are ver# sensitive tosunlight &eing in the sun for even a shorttime can cause a painful rash (ome peoplewith (5/ can even get a rash fromfluorescent lights
+ashes caused b# (5/ are red, itch#, andpainful 8he most t#pical (5/ rash is calledthe butterfly rash, which appears on theface 0 particularl# the cheeks and across thenose (5/ can also causes hair loss 8he hairusuall# grows back once the disease isunder control
Lupus Anatomy ("oints Almost ever#one with (5/ has joint pain
or inflammation An# joint can beaffected, but the most common spots arethe hands, wrists, and knees 9suall# the
j i t b th id f th b d
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same joints on both sides of the bod# are
affected 8he pain can come and go, or itcan be long lasting 8he soft tissuesaround the joints are often swollen, butthere is usuall# no e!cess fluid in the
joint "an# (5/ patients describe musclepain and weakness, and the muscletissue can swell
Lupus Anatomy 5upus can also affect the nervous s#stem causing
headaches, sei:ures, and organic brain s#ndrome
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It can cause anemia due to blood loss or from thdisease it does not directl# effect the red blood
regnanc#% the chances of miscarriage, prematuand death of the bab# in the uterus are high
#erone$ati%e #pondyloarthropa $onsist of a group of related
disorders that include +eiter3ss#ndrome, ank#losing spond#litis,psoriatic arthritis, and arthritis in
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p
association with inflammator# boweldisease ;ccurs more age at diagnosis in the
third decade and a peak commonl#among #oung men, with a meanincidence between ages < and =4
8he prevalence appears to be about1>
8he male-to-female ratio approaches4 to 1 among adult $aucasians
?enetic factors pla# an importantrole in the susceptibilit# to eachdisease
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#erone$ati%e #pondyloarthropa 8he spond#loarthropathies share certain common features, including
of serum rheumatoid factor, an oligoarthritis commonl# involving larthe lower e!tremities, freuent involvement of the a!ial skeleton, faclustering and linkage to @5A-&<7
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clustering, and linkage to @5A &<7
8hese disorders are characteri:ed b# inflammation at sites of attachligament, tendon, fascia, or joint capsule to bone enthesopath#2
#acroiliitis (acroiliitis is an
inflammation of thesacroiliac joint ( t ll i l d
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(#mptoms usuall# include afever and reduced range ofmotion
icture on the bottomright shows an individualwith 0 sacroiliitis andAnk#losing (pond#litis
8he arrows point to theinflamed and narrowed (I joints 8he# are whitedue to bon# sclerosisaround the joints
An&ylosin$ #pondylitis $hronic disease that primaril#
affects the spine and ma# leadto stiffness of the back 8he
joints and ligaments thatnormall# permit the back to
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normall# permit the back to
move become inflamed 8he joints and bones ma# growfuse2 together
8he effects are inflammationand chronic pain and stiffnessin the lower back that usuall#starts where the lower spine is
joined to the pelvis or hip
iagnosis is made through%a2 medical histor# includings#mptoms, b2 B-ra#s, andpossibl# c2 blood tests for@5A-&<7 gene
An&ylosin$ #pondylitis 8reatment options%
Cith earl# diagnosis and treatment,pain and stiffness can be controlledand ma# reduce fusing In women, A(
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and ma# reduce fusing In women, A(
is usuall# mild and hard to diagnose /!ercise
"edications% (AIs, (ulfasala:ine osture management
(elf-help aids
(urger#
Reiter's #yndrome Arthritis that produces pain, swelling, redness and heat i
joints It can affect the spine and commonl# involves thethe spine and sacroiliac joints It can also affect man# otof the bod# such as arms and legs "ain characteristic fe
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of the bod# such as arms and legs "ain characteristic feinflammation of the joints, urinar# tract, e#es, and ulceraskin and mouth
8he s#mptoms are fever, weight loss, skin rash, inflammsores, and pain
Reiter's #yndrome +eiter3s often begins following
inflammation of the intestinal or urinar#tract It sets off a disease processinvolving the joints, e#es, urinar# tract,and skin "an# people have periodic
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and skin "an# people have periodicattacks that last from three to si!months (ome people have repeatedattacks, which are usuall# followed b#s#mptom-free periods
iagnosis is made through a ph#sicale!am, skin lesions, and a test for the
@5A-&<7 gene
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Psoriatic Arthritis iagnosis ma# involve B-ra#s, blood
tests, and joint fluid tests 8reatment options%
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(kin care 5ight treatment 9.& or 9.A2 $orrective cosmetics "edications% glucocorticoids, (AIs, "A+s
disease-modif#ing anti-rheumatic drugs2 /!ercise +est
@eat and cold (plints (urger# rarel#2
Scleroderma (Systemic sclerosis)
Definition: progressive sclerosis of skin andconnective tissue; fibrous and vascular chanskin, blood vessels, muscles, synovium, inte
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organs. become “hide bound” Immune-mediated disorder; genetic compo
Scleroderma (Systemic sclerosis)
bnormal amounts of fibrous connective tisdeposited in skin, blood vissels, lungs, kidneother organs
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!an be systemic or locali"ed #!$%&'( syndr
CREST Syndrome
!alcinosis
$aynaud)sphenomena
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phenomena
%sophagealhypomotility
&clerodactyl#skin changes offingers(
'elangiectasia#macula-likeangioma of skin(
More on CRES
T
2rest 'yndrome
CREST Syndrome & scleroderma
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&clerodactyl#locali"edscleroderma offingers(
+a#naud's diseasewith ischemia
Manifestations &
Complications (systemic)
*emale +: ain, stiffness,
polyartheritis
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ausea,vomiting
!ough /ypertension $aynauld)s
syndrome Skin atrophy,hyperpigmented
Scleroderma cont.
%sophagealhypomotility leadsto fre0uent reflu1
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0
2I complaintscommon
3ung-pleuralthickening andpulmonary fibrosis
$enal disease...leadingcause of death4
Diagnosis/Treatment
Scleroderma $56 autoimmune
disease
$adiological:pulmonary fibrosis,
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bone resorption,subcutaneouscalcification, distalesophagealhypomotility
%&$ elevated
CBC anemia Gammaglobulin lelels
elevaed; RA present
Skin biopsy to confirm
Scleroderma: Patient Care
Do)s void cold
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rovide small, fre0uentfeedings
rotect fingers
&it upright post meals
o fingersticks
Daily oral hygiene
Scleroderma: Patient Care
7edications: based upon
symptoms:
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Immunosuppressive agents steroids remitting agents
Ca channels blockers alpha!adrenergic blockers
"# receptor blockers
AC$ inhibitors Broad spectrum antibiotics
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Thank Cou