REMATHOID ARTRITIS, by Sigit Purwanto

1. REMATOID ARTRITIS
Disampaikan pada perkuliahan KMB II di PSIK FK Unsri
Sigit Purwanto, S.Kep.,Ns

2. PENGERTIAN
1. Rheumatoid arthritis (RA) is an autoimmune disease that
causes chronic inflammation of the joints. Rheumatoid
arthritis can also cause inflammation of the tissue around
the joints, as well as in other organs in the body.
2. Rheumatoid arthritis (RA) atau sering juga disebut artritis
reumatoid (AR) merupakan salah satu jenis penyakit
rematik yang merupakan penyakit autoimun

3. 3. Salah satu bagian dari poliartritis yang menimbulkan
anflamasi ditandai dengan perjalanan klinik yang
bervariasi tetapi biasanya disertai eksaserbasi dan remisi
nyeri serta pembengkaan sendi yang dapat menyebabkan
deformitas progresif
4. Gangguan kronik yang menyerang berbagai sistem organ
yang biasanya menyebabkan destruksi sendi.

4. RHEMATOID ARTRITIS
Sering disebut rematik/artritis atau peradangan pada
sendi.
Penyakit ini terutama mengenai otot skelet, tulang,
ligamentum, tendon dan persendian
Mengenai laki-laki dan perempuan di segala usia, dengan
perempuan lebih sering 3 x.
Sering menyerang sendi kecil dan simetris

5. It occurs worldwide, affecting more than 6.5 million
people in the U.S. alone.
About 75 % of these are women.
The disease strikes women three times more often
than men.
RHEUMATOID ARTHRITISRHEUMATOID ARTHRITIS

6. Although it can occur at any age, the peak onset
period is between the ages of 35 and 50.
The disease may come on slowly or may appear
suddenly.
RHEUMATOID ARTHRITISRHEUMATOID ARTHRITIS

7. At Risk
It affects around
1.3 million
Americans, which
70 of are women.
Although it can
occur at virtually
any age
People between the
ages of 30 -50 yrs
3
1

8. Rheumatoid Arthritis
RA
Synovial
membrane
Cartilage
Capsule
Synovia
l
fluid
Inflamed
synovial
membrane
Pannus
Major cell types:
• T lymphocytes
• macrophages
Minor cell types:
• fibroblasts
• plasma cells
• endothelium
• dendritic cells
Major cell type:
• neutrophils
Cartilage thinning

12. ETIOLOGI

13. ETIOLOGY OF RAETIOLOGY OF RA
The cause of rheumatoid arthritis is unknown. Even though
infectious agents such as viruses, bacteria, and fungi have long
been suspected as well as smoking, but none has been proven
as the cause.
It is believed that the tendency to develop rheumatoid
arthritis may be genetically inherited.

14. ETIOLOGY OF RAETIOLOGY OF RA
For example, the genetic marker HLA-DR4 has been
identified in as many as 66% of patients with disease.
This marker, which is present in white blood cells, plays a
role in helping the immune system to distinguish
between foreign cells (e.g., germs) and the body's own
cells.
Because RA often is affected by pregnancy—symptoms
improve before the infant is born and then worsen after
delivery—it may be that hormones in the body influence
disease development and progression.

15. PATOFISIOLOGI
Penyakit autoimun yang menyerang persendian, terutama sendi
kecil seperti tangan & kaki secara simetris, mengalami
peradangan kemudian sendi mengalami kerusakan. Kerusakan
mulai terjadi 6 bl pertama serangan, cacat bisa terjadi setelah 2-3
th bila tidak diobati.
autodigesti terjadi karena gangguan pada fungsi normal dari
sistem imun atau dikarenakan adanya kegagalan antibodi dan sel
T untuk mengenali sel tubuhnya sendiri sehingga merusak sel
tubuh sendiri karena menganggap sel tubuh merupakan benda
asing.

16. PATOFISIOLOGI lanjutan
Menyerang lapisan dalam bungkus sendi (sinovium) yang
mengakibatkan radang pada pembungkus sendi. Akibat
sinovitis yang menahun, akan terjadi kerusakan pada tulang
rawan sendi, tulang, tendon & ligamen dalam sendi.
Peradangan sinovium menyebabkan keluarnya beberapa zat
yang menggerogoti tulang rawan sel sehingga menimbulkan
kerusakan tulang dan dapat berat

17. Cells of the Immune System
Basophils
Neutrophils
Eosinophils
Granulocytic
Langerhans &
Macrophages
Kupffer cells
Dendritic cells?
Monocytic
Cytotoxic
Helper
Suppressor
T-cells
Plasma
cells
B-cells Dendritic
cells?
lymphoid cells
Myeloid cells

18. Destruksi jaringan sendi
1) Destruksi pencernaan oleh produk protease, kolegenase
dan enzim hidrolitik. Enzim tersebut berperan dalam
memecah tulang rawan, ligamen, tendon dan tulang pada
sendi yang dilepaskan bersamaan dengan radikal oksigen
dan asam arakhidonat oleh leukosit polimorfonuklear
dalam cairan sinovial.
2) Destruksi jaringan melalui kerja panus rhematoid. Panus
merupakan jaringan granulasi vaskular yang terbentuk
dari sinovium yang meradang yang kemudian meluas ke
sendi.

19. Apa beda OA dengan RA

20. OSTEOARTRITIS RHEMATOID ARTRITIS
identifikasi kerusakan sendi tulang rawan
sendiri & pertumbuhan tulang
berlebihan.
peradangan pada selaput
sinovial hingga tulang rawan
hancur.
lokasi sering jari-jari, tangan atau
lutut.
masuk tubuh dengan gejala di
lebih dari satu bidang.
imun Tidak mengenai sistem
kekebalan tubuh.
penyakit autoimun, kekebalan
tidak berfungsi semestinya
Usia & JK > 40 tahun mengenai sama
antara laki dan perempuan.
setiap usia (20 - 60 th) dan
lebih sering pada wanita.
problem Dapat disebabkan oleh
obesitas, tekanan berulang-
ulang pada sendi.
tidak diketahui, tidak
disebabkan oleh gaya hidup.
considerations penyakit umum yang merusak
sendi.
Jarang terjadi tapi lebih serius

21. LOKASI SENDI YANG SERING BERMASALAH

22. The synovium red due to blood vessel
diatations and thickened due to
inflammation and cellular infiltration.
Plus granulations form over the
synovial membrane now called as
pannus.
Rheumatoid Arthritis

24. TANDA DAN GEJALA
o Kelelahan
o kehilangan energi
o Anoreksia,
o BB menurun
o Demam ringan,
o Sakit otot dan sendi, dan kekakuan terutama pagi hari.
o Kesulitan ADL ; memutar kenop pintu, membuka botol
o Bila mengenai sendi kecil kaki ; sakit saat jalan di pagi hari
saat bangun tidur
o Scleritis, peluritis, anemia, nodul rematoid, vaskulitis,
nekrosis

25. o Poliartritis simetris terutama sendi perifer termasuk tangan
o Deformitas
o Nodula rhematoid
o Deformitas yang dapat menyebabkan penurunan
kemampuan bergerak terutama saat ekstensi
TANDA DAN GEJALA

26. PENGKAJIAN
Riwayat kesehatan umum
Riwayat keluarga
Cara berjalan, struktur, ukuran muskuloskeletal
Aktivitas yang masih dapat dilakukan
Penyesuaian yang telah dilakukan oleh pasien
Perubahan fungsional

27. DATA DASAR PENGKAJIAN
Nyeri sendi saat bergerak, nyeri tekan, kekauan pada pagi
hari, limitasi fungsional, keletihan
Fenomena Tynaud jari dan tangan (pucat intermitten,
sianosis, kemerahan pada jari)
Ketergantungan pada orang lain
Anoreksia, nausea, vomiting, kesulitan mengunyah.
Kebas/kesemutan pada tangan dan kaki sampai hilangnya
sensasi
Nyeri akut dengan /tanpa bengkan jaringan lunak, nyeri
kronis dan kekakuan terutam pad pagi hari.
Kulit mengkilat, tegang, nodul subcutaneus, kekeringa
membran mukosa

28. Kulit
ruang/lesi, peningkatan memar, eritema, penipisan,
panas/hangat, fotosintesis
Rambut
alopecia/penipisan
Mata
kering/kasar, penurunan ketajaman, katarak, penurunan
daya penglihatan perifer, konjungtivitis/uveitis
Telinga
tinitus, penurunan tajam pendengaran

29. Mulut
lesi pada pipi/sublingual, perubahan daya pengecap, kering,
disfagia, kesulitan pengunyah
Dada
nyeri pleuritik, penurunan ekspansi dada, Intoleransi
aktivitas (dispnea)
Sistem KV
jari tangan pucat saat dingin, pulsus perifer
Abdomen
perubahan defekasi, mual/muntah, meteorismus, nyeri,
perubahan berat badan

30. Genetalia
kering/gatal, haid abnormal, perubahan kinerja seksual,
higiene, uretritis dan disuria, lesi
Neurologik
paraestesia ekstrimitas, corak refleks yang abnormal, sakit
kepala.
Muskuloskeletal
kemerahan sendi/hangat/bengkak/nyeri tekan atau
deformitas, rentang gerak sendi, gambaran jaringan
atropi/nodul subkutan, kista poplitea, kekuatan otot.

31. Nilai laboraturium
LED meningkat pesat (80 – mm/h), hitung darah lengkap
(anemia), trombosit, kadar salisilat, leukositosis
X ray
hilangnya kartilago, penyempitan rongg sendi, abnormalitas
kartolago, erosi sendi, pertumbuhan tulang yang abnormal,
osteopania
PEMERIKSAAN LABORATORIUM

32. Pemindaian tulang
mencerminkan derajat pengambilan absorbsi isotop
radioaktif oleh jaringan tulang.
Biopsi
b. arteri u memeriksa spesimen arteri, biopsi kulit u
memastikan inflamasi jaringan ikat
PEMERIKSAAN LABORATORIUM

33. Perbedaan photo x-Ray normal dan Rheumatoid
Arthristis
Stephen Luce

34. Diagnostic Criteria for RA
≥ 4 criteria present > 6 wks
Morning stiffness > 1 hour
Arthritis of ≥ 3 joints areas
(PIP, MCP, wrist, elbow,
knee, ankle, and MTP)
Arthritis of hand joints
(wrist, MCP, PIP)
Symmetric arthritis
Rheumatoid nodules
RF+
Radiographic changes
 Erosions
 Unequivocal periarticular
osteopenia

36. DIAGNOSA KEPERAWATAN
Nyeri b.d inflamasi dan peningkatan aktivitas penyakit,
mudah lelah, keterbatasan aktivitas
Keletihan b.d peningkatan aktivitas penyakit, nyeri,
tidur/istirahat yang tidak memadai, dekondisioning, nutrisi
yang tidak memadai
Kerusakan mobilitas fisik b.d penurunan ROM, kelemahan
otot, nyeri pergerakan, keterbatasan ketahanan fisik,
kurangnya/tidak tepatnya penggunaan alat-alat ambulatori.

37. Kurang perawatan diri b.d kontraktur, keltihaan atau
gagngguan gerak
Gg citra tubh b.d perubahan atau ketergantungan fisik serta
psikologis karena penyakit atau terapi
Koping tidak efektif b.d gaya hidup atau perubahan peranan
yang aktual atau yang dirasakan.

38. PENATALAKSANAAN
Memberikan obat anti inflamasi
Melindungi sendi, meredakan nyeri dengan bidai, terapi suhu,
relaksasi
Mengimplementasikan latihan ROM dan penguatan otot
Menggunakan sarana atau teknik adaptasi
Menyampaiakn dan menyegarkan kembali informasi yang
diajarkan kepada pasien.
Meningkatakn penatalaksanaan mandiri oleh pasien yang
kompatibel dengan program terapi

39. PENGOBATAN
The first-line drugs,
aspirin and cortisone (corticosteroids)
The slow-acting second-line drugs,
methotrexate (Rheumatrex, Trexall),
hydroxychloroquine (Plaquenil), promote disease remission
and prevent progressive joint destruction, but they are not
anti-inflammatory agents.

40. Salisilat
aspirin, kolin salisilat, salsalat, kolin Magnesium trisalisilat.
NSAIDs
ibuprofen, ketoprofen, oksaprofen, meklofe- namat,
fenilbutason, piroksikam, diklofenak, indometasin.
Antirematik kerja lambat
penisilamin, klorokuin, hidroksiklorokuin
Preparat imunosupresi
metotreksat, azatioprin, siklosfofamid
Kortikosteroid
prednison, prednisolon, hidrokortison

41. INTERVENSI KEPERAWATAN
Meredakan nyeri
- preparat analgetik seperti asetaminopen
- strategi koping yang memungkinkan
- program penurunan berat badan
- kompres hangat bisa mandi rendam/siram
- kompres dingin untuk nyeri akut
- penggunaan verban tekan, bidai & alat bantu mobilisasi
- Dorong pasien mengutarakan nyerinya
- jelaskan patofisiologi nyeri pasien
- lakukan penilaian terhadap perubahan subyektif pada
nyeri

42. Mengurangi keletihan
- istirahat, pemakaian bidai, mbatasi gerakan & stres pd sendi
- mandi hangat dan penggunaan teknik teknik relaksasi
- lantihan kondisoning ; bersepeda, jalan, berenang
Meningkatkan tidur restoratif
Meningkatkan mobilitas
- pengaturan posisi tubuh yang tepat ; terlentang, duduk.
- latihan gerak aktif maupun pasif
- perhatikan pemasangan bidai yang tepat
- penggunaan alat-alat bantu jalan.
Memperbaiki citra tubuh

43. HAWO TO LIFE A NORMAL LIFESTYLE
 Connect with others, as in your family make them aware of how you’re
feeling. Find a family member or friend you can talk to when you’re feeling
overwhelmed
 Take time for yourself. Its easy to get caught up in the busy world but
dont’t forget to take time for yourself, travel, go for a walk, listen to your
favorite music.
 Know your limits. Your body knows when its oudone itself and need to
recharge, so let it. A rest or short nap that doesn’t interfere with your
regualr sleep schedule.

44. HoW TO LIFE A NORMAL LIFESTYLE
 Exercise regularly, certain excersise can help strengthen the muscles
around the joints and promote growth. So take a short walk, go swimming.
 Take controle, in other words make a plan for how you going to manage
your arthritis. This will help you feel in charge of your disease.
 Apply heat or cold. Heat helps ease the pain and relax tense, painful
muscles.. Cold may lessen the sensation of pain but it also decreases
muscle spasms.

45. COMPLICATIONS OF RHEUMATOID ARTHRITISCOMPLICATIONS OF RHEUMATOID ARTHRITIS
Swan neck deformities
Boutonniere deformities
Z deformity of thumb
Bow string sign
The tendons on the back of the hand may become very
prominent and tight, called the bow string sign.

46. Swan neck deformity
The deformity
arises from
hyperextension
of the proximal
interphalangea
l joint, while
the distal
interphalangea
l joint is flexed.

48. Swan neck
FDS rupture/
volar plate
injury
Lateral bands
sublux dorsally
PIP
hyperextends
and DIP flexes

51. Buttonhole DeformityButtonhole Deformity

52. Boutonniere deformity
Flexion of the PIP joint accompanied by hyperextension of the DIP joint is
boutoniere deformity in little finger.
Flexion of the PIP joint accompanied by hyperextension of the DIP joint is
boutoniere deformity in little finger.

54. Boutoniere deformityBoutoniere deformity

55. Z-deformityofThumb

56. Bow string signBow string sign
The tendons on the back
of the hand may become
very prominent and
tight, called the bow
string sign.
Ulnar deviation
The direction of
prominent tendons is
like bow string

57. Rheumatoid nodulesRheumatoid nodules
Painless firm lumps that
appear beneath the skin,
often single or multiple,
and range in size from
millimeters to centimeters
in diameter occur on the
underside of the forearm
and on the elbow.

58. Rheumatoid nodulesRheumatoid nodules
But they can also occur on
other pressure points,
including the back of the
head, the base of the
spine, the Achilles tendon,
and the tendons of the
hand

59. Rheumatoid nodulesRheumatoid nodules
Occur in about 25% of
patients
More common in men
than women

60. Rheumatoid nodulesRheumatoid nodules
Although nodules are
mostly benign,
complications such as
infection, ulceration, and
gangrene can occur
following breakdown of
skin overlying the
nodules.

61. Skin complications of RASkin complications of RA
Skin and
muscles
become
atrophic (thin
and
wrinkled),
making it
fragile and
easy to bruise

62. Skin complications of RASkin complications of RA
Skin on the
back of the
hands may
become pale
or even
translucent
Nails may
become brittle
and split
length-wise

63. Skin complications of RASkin complications of RA
The palms
become
reddened
(palmer
erythema)

64. Skin complications of RASkin complications of RA
Dark purplish
areas on the
skin (purpura)
are caused by
bleeding into
the skin from
blood vessels
damaged by
rheumatoid
arthritis.

65. Skin complications of RASkin complications of RA
Rheumatoid
Vasculitis can
cause many
internal
symptoms, ,
hepatomegaly
(enlarged liver),
splenomegaly
(enlarged spleen),
bowel ulcers, and
haematuria (blood
in urine).

66. RA - VasculitisRA - Vasculitis

67. RA - VasculitisRA - Vasculitis

68. Skin complications of RASkin complications of RA
Skin ulcers
(usually leg ulcers)
may be extensive
and painful
Petechiae
(purplish spots) or
purpura
Nail fold or edge
breakdown
Gangrene

69. Skin complications
of RA
Skin complications
of RA
Neutrophilic
dermatoses
Neutrophils are a
type of white blood
cell (leucocyte).
They are present in
bacterial infections.
They are the
prominent cell seen
on skin biopsy of
some uncommon
inflammatory skin
diseases known as
neutrophilic
dermatoses.

70. Skin complications
of RA
Skin complications
of RA
Sweet disease
and pyoderma
gangrenosum are
other
neutrophilic
disorders
sometimes seen
in association
with rheumatoid
arthritis.
Pyoderma
gangrenosum

71. Skin complications
of RA
Skin complications
of RA
Interstitial
granulomatous
dermatitis.
also known as
‘rheumatoid
papules’, interstitial
granulomatous
dermatitis presents
as skin coloured or
red papules often on
the trunk. It is rare.

72. Skin complications
of RA
Skin complications
of RA
RA can affect the
glands located near
the eyes and
mouth, resulting in
a condition called
secondary
Sjögren's
syndrome.
Decreased tear and
saliva production
can cause dry
mouth, and dry
eyes.

73. GASTRO-INTESTINAL COMPLICATIONSGASTRO-INTESTINAL COMPLICATIONS
Dry mouth, related to Sjogren syndrome, is the most
common symptom of gastrointestinal involvement.
Gastritis (stomach inflammation) or stomach ulcer
caused by NSAID therapy.

74. Nervous complications of RANervous complications of RA
Entrapment of
nerves. Carpal
tunnel
syndrome or
ulnar nerve
neuropathy
 including
sensory or
motor
neuropathy
(loss of
sensation)

76. Nervous complications of RANervous complications of RA
Formation of a Baker's
cyst (a cyst filled with
joint fluid and located in
the hollow space at the
back of the knee).
Its herniation of
posterior capsule

77. OCULAR COMPLICATIONS OF RAOCULAR COMPLICATIONS OF RA
RA can also cause
inflammation of the
sclera (white part of the
eye), which may make
the sclera appear red or
bluish in color.

78. OCULAR COMPLICATIONS OF RAOCULAR COMPLICATIONS OF RA
Keratoconjunctivitis
sicca

79. OCULAR COMPLICATIONS OF RAOCULAR COMPLICATIONS OF RA
Episcleritis

80. OCULAR COMPLICATIONS OF RAOCULAR COMPLICATIONS OF RA
Scleritis

81. OCULAR COMPLICATIONS OF RAOCULAR COMPLICATIONS OF RA
Stromal corneal
opacities with peripheral
vascularisation

82. OCULAR COMPLICATIONS OF RAOCULAR COMPLICATIONS OF RA
Iridocyclitis.

83. OCULAR COMPLICATIONS OF RAOCULAR COMPLICATIONS OF RA
Marginal thinning of the
cornea with keratolysis

84. Lysis of bonesLysis of bones
Punched out lytic
changes in bones

85. Lytic changes in
toes

86. RA - kneesRA - knees
Joint spaces in knee is
reduced due cartilage
destruction.

87. Cock-up deformity or hammer toesCock-up deformity or hammer toes

88. MTP SubluxationMTP Subluxation
Abducto hallus vulgus

89. MCP SubluxationMCP Subluxation
Subluxation of MCP
joints.

90. Ulnar DeviationUlnar Deviation

93. TERIMA KASIH