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PHARMACEUTICAL CARE

PADA RHEUMATOID ARTHRITIS


Rheumatoid arthritis
 Gangguan inflamasi sistemik kronik persisten,
ditandai dgn potentially deforming polyarthritis ,
inflamasi sendi simetris dan manifestasinya
ekstra artikular luas
 Autoimmune disease

 Dlm jk lama tjd erosi tlg, destruksi tulang rawan,


hilangnya integritas sendi scr keseluruhan,-
sistem multiple organ dpt dipengaruhi 
→rheumatoid nodules, vasculitis, inflamasi
mata, neurologic dysfunction, cardiopulmonary
disease,lymphadenopathy, splenomegali

Etiologi
genetik, lingkungan, penambahan usia, sistem
immune
Kriteria diagnosis RA

1. Morning stiffness in and around joint lasting ≥ 1 hr before


maximal involvement
2. Soft tissue swelling (arthritis) of ≥ 3 joint areas
3. Swelling (arthritis) of the proximal interphalangeal,
metacarpophalangeal, or wrist joints ( sendi perge-
langan)
4. Symmetric arthritis
5. Subcutaneous nodules
6. Positive test for rheumatoid factor (RF)
7. Radiographic erosions or periarticular osteopenia in
hand or wrist joints
 Patofisiologi

(1) Destruksi sendi (inflamasi lapisan sinovial )

lapisan tipis ruang sendi, berproliferasi (menebal) dan


terbentuk pannus sinovial (erosif)

invasi articular cartilage ( penyempitan ruang sendi (+)),


mengerosi tulang (osteoforosis (+)) & hancurkan struktur
periartikuler (ligament,tendon)

deformitas sendi (+)


(2) Sel imun (limfosit T atau B) bereaksi dgn protein yg
berkembang di thymus atau sumsum tulang

lepas dari destruksi ( terbunuh atau terinaktivasi )

teraktivasi bbrp tahun & timbul respon autoimun


(aktivasi disebabkan bakteri (Streptococcus) or virus (mengandung
protein dg AA serupa protein jar)

sumber aktivasi (self – targeted immune cell) capai sendi

komplek sel-sel (+)

RA (+)
 Terapi
- Guidelines terapi RA dipublikasikan o/ American
College of Rheumatology
-No treatment cures rheumatoid arthritis
-The therapeutic goals :
a.Remission of symptoms involving the joints
b.Return of full function
c.Maintenance of remission with DMARD therapy.

DMARD : disease modifying anti rheumatic drug


PROBLEMA MEDIK
Problema medik pd RA hampir sama dgn OA :
1. Joint pain,stiffness,inflamation
2. CKD
3. Chirrosis hepatic
4. Diabetes mellitus
5. Cardiovascular disease (hypertension, HF dll)
6. Peptic ulcer disease
7. Melena
8. Anemia
9.Thrombocytopenia
10. Infection
1. Joint pain,stiffness,inflamation
Pengatasan nyeri, kekakuan dan inflamasi sendi
diterapi dgn :
a. Non farmakologi
- Regular exercise (minimalkan atrofi otot dan
kontraktur flexion, jaga fgs sendi), proteksi sendi
dan konservasi energi, emotional support

-Rest, occupational therapy, physical therapy,


penggunaan alat bantu, weight reduction, surgery
( tenosynovectomy, tendon repair, joint replace-
ments )
b. Farmakologi
- DMARDs should be started within the first 3 months of
symptom onset
- Guideline terbaru : as soon as possible

- Early introduction of DMARDs results in a more


favorable outcome and can reduce mortality

- + NSAIDs and / or corticosteroids may be used for


symptomatic relief rapid improvement in symptoms
 DMARDs
-Turunkan inflamasi sendi, turunkan atau cegah kerusakan
sendi, pelihara fgs sendi dan integritasnya
- Segera digunakan utk minimalkan loss of joint integrity
and function dan risiko peny. kardiovaskuler krn RA
-- Bila dgn terapi tunggal MDARD tdk berhasil  tx
kombinasi
- Monoterapi : MTX, leflunomida
- Dikombinasi dg NSAID lbh efektif dp monoterapi
- Obat : hydroxychloroquin, sulfasalazine, MTX,lefluno-
mide, gold, azathioprine, D-penicillamine
- Methotrexate (immunosuppressive and anti-inflammatory)
 superior clinically outcomes than the other DMARDs,
lower cost than biologic agents, reduction in cardiovas-
cular morbidity and mortality

-OOA DMARD lambat (3-6 bln),efek manfaatnya dlm 1-2


bln

-tdk blh diberikan pd px dg infeksi aktif, rwyt kekambuhan


infeksi,predisposisi thd infeksi  imunosupresif

- Tdk
direkomendasikan pd HF sedang ad berat, hati-hati pd
mild HF
- HCQ, MIN, or SSZ →mild cases of RA
- The mechanism of anti-inflammatory effect of
HCQ :
- inhibition of migration of neutrophils and eosino-
phils, histamine and serotonin blockade, or inhibi-
tion of prostaglandin synthesis
- Sulfasalazine : induce anti-inflammatory effects
through one of its active metabolites, mesalamine,
which is believed to inhibit both COX and
lipoxygenase
 Biologic agents
- It targeted to proinflammatory cytokines (TNF-α
and IL-1,IL-6,IL-8 ) →immunopathogenesis of RA
- Effective for patients who fail treatment with other
DMARDs
- Obat anti-TNF etanercept, infliximab,
adalimumab,certolizumab,golimumab
- Costimulation modulator abatacept
- Rituximab depletes peripheral B cells
 Less frequently used
- less efficacy, high toxicity
* IL-1 receptor antagonist : anakinra
* Azathioprine, D-penicillamine, gold (auranofin), minocy-
cline, cyclosporine ,cyclophosphamide
- AZA :
*for patients with severe disease who do not
respond to safer alternatives
*ESO : myelosuppression,hepatotoxicity
- Cyclosporine :
* for severe, refractory RA
* ESO : renal insufficiency ,hypertension
- Cyclophosphamide and chlorambucil :
* effective in the treatment of severe progressive
RA
* It has potentially serious toxicity (e.g.,
malignancy,
infections)
* It is limited to patients with progressive RA
unresponsive to more conservative management
* for potentially life-threatening complications of
RA (e.g., rheumatoid vasculitis).
- Infliximab + MTX to prevent development of
antibodies that may reduce drug efficacy or
induce allergic reactions
- Combination therapy (two or more DMARDs ) 
effective when single-DMARD treatment is
unsuccessful
-cyclosporine + MTX , MTX + sulfasalazine +
hydroxy-chloroquine  effective
- Switching among DMARDs
* If after 3 months of DMARD monotherapy ( patients
without poor prognostic features)  develop to
deteriorates from low to moderate/high disease activity
+ MTX,HCQ, or leflunomide

* If after 3 months of MTX or MTX/ DMARD combination


patient still has moderate or high disease activity  +
another non-MTX DMARD or switch to a different non-
methotrexate DMARD
- Switching from DMARDs to biologic agents
* Moderate or high disease activity after 3
months of MTX monotherapy or DMARD
combination therapy  add or switching to an
anti TNF biologic, abatacept, or Rituximab

* After 3 months of intensified DMARD


combination or after a second DMARDstill has
moderate or high disease activity add or
switch to an anti-TNF biologic
 Hydroxychloroquine
~sering dipakai walau kurang poten
~for low RA, good prognose
~inhibition of migration of neutrophils and eosi-
nophils, histamine and serotonin blockade, or
inhibition of PG synthesis
~Partially metabolized in the liver and is excreted
by the kidney
~ Lack of myelosuppressive,hepatic, and renal
toxicities
~ Safe in pregnancy
~ ESO
- retinopathy (>800 g)
-gastrointestinal effects ( nausea,vomiting,
diarrhea), ocular toxicity ( blurred vision), night
blindness
- neurologic adverse effects (headache, vertigo,
and insomnia ~ aritmia dosis tinggi
~ dosis : 400-600 mg/hari ( 310-465 mg base),dosis
rumatan(155-310 mg base) < 24 bln )
* Methotrexate
~ Now considered the DMARD of choice for treating
severe RA
~ Antiinflammatory properties inhibits cytokine produc-
tion, inhibits purine biosynthesis, folic acid antagonist
,stimulate release of adenosine
~ rapid onset (1-2 bln), efikasi tinggi
~ Dosis : p.o 7,5 mg /minggu atau 3x2,5 mg/hari/mgg.Dpt
ditingkatkan 15mg/mgg (atau 3x5 mg) slm 12 mgg.
~ Toxicities mainly GIT,hematologic,hepatic ,mukositis,
alopecia ringan, myelosupression, pneumonitis, hepatic
fibrosis, CH, pe ↑ enz transaminase(> 3x)
~ It may be given i.m, s.c, or orally
~ + an as folat  cegah gangguan sal cerna ,
mukositis, alopesia krn MTX.
~ as. Folat (1 mg/hari) or folinic acid 2,5 mg/mgg
(leucovorin) dpt turunkan ALT
~ MTX +HCQ →moderate to high disease activity
,low disease activity and disease > 24 months
~ MTX + SSZ is → for poor prognosis and all
disease durations
~ MTZ +HCQ+SSZ →moderate to high disease
activity levels and poor prognosis
- Interaksi obat
~ NSAID tingkatkan consent MTX serum  toks
(adjust dosis)
~ dg trimetropin tingkatkan MTX induce supresi
bone marrow
*Azathioprine
~Utk severe RA,cadangan bila tx lain yg lebih
aman tdk berrespon
~Dosis 1 mg/kg/hari (single, terbagi). Dpt diting-
katkan 0,5 mg/kg/hari stlh 6-8 mgg. MD 2,5
mg/kg/hari.
~ ESO: gangg GI,myelosupression, hepatotoxicity
~ + allopurinol : metab & eliminasi AZA 
toksisitas me ↑  adjust dosis ad 75%
 Cyclosporine
- For severe, refractory RA
- Inhibition of production and release of IL-II and
inhibit IL-II induced activation resting T-lympho-
cytes
- ESO : renal insufficiency, hypertension, female
reproductive disorder
- Monitor : kadar Cr, TD
* Sulfasalazine
~ prodrug, is diubah oleh bakteri di kolon jd sulfapyridine
dan 5-aminosalicylic acid
~ anti rheumatic the exact mechanism of action is
unknown (active metabolites mesalamine →inhibit
COX and lipoxygenase )
~onset > cpt dp HCQ (1 bln),efek anti RA terlihat dlm 2 bln,
respon klinik bertahan ad 4 bln
~ESO :skin rash, leukopenia, trombositopenia alopecia,
stomatitis, elevated hepatic enzymes
~ May cause the patient’s urine and skin to turn a yellow-
orange color
~ Dosis : awal 500 mg/hari atau 1 g/hari dan ditingkatkan
500-1000 mg tiap mgg ,2-3 x sehari.
 Leflunomide
-Inhibits pyrimidine synthesis to decrease in
lymphocyte proliferation and modulation of
inflammation.
- The efficacy similar to MTX
-Contraindicated in patients with preexisting liver
disease  liver toxicity
-Teratogenic
- Bone marrow toxicity
- Antidotum : Cholestyramine
 Agen biologis
- Bekerja pd cytokines proinflammatory spt TNF - (infli-
ximab, etanercept, adalimumab, golimu-mab, and
certolizumab), IL-1 ( IL-1, IL-1) (ana-kinra), dan IL-
6 (tocilizumab), deplete peripheral B cells
(rituximab), or bind to CD80/86 on T cells to
prevent the costimulation needed to fully activate
T cells (abatacept)
- effective when other DMARDs fail to achieve adequate
responses
- Penggunaan mono or komb dg MTX lbh cepat
perbaiki gjl & symptom serta perlambat progre-
sifitas RA dp DMARD
- Utk moderate to severe diasease
- Efikasi jk lama blm tahu
 Efek samping
- sekunder sepsis, TBC, infeksi mycobacterium
atypical, infeksi jamur, infeksi oportunistik
tjd pd px dg DM tak terkontrol , tx bersamaan dg
kortiko atau DMARD

- tdk blh diberikan pd px dg infeksi aktif, rwyt


kekambuhan infeksi,predisposisi thd infeksi.
- tdk direkomendasikan pd px HF moderate to
severe, caution pd mild
-Terapi kombinasi
~ pengawalan kombinasi tx percepat outcome px
ok erosi sendi tjd pd 2 thn pertama.
~Komb MTX, HCQ, SSZ sgt efektif.
~NSAID digunakan sbg tx tambahan utk relief
simptomatik
 NSAID
-It possess both analgesic and antiinflammatory
properties and reduce stiffness associated with
RA
-Utk relief nyeri dg cepat dan turunkan inflamasi
sendi
-It seldom be used as monotherapy  they do not
alter the course of the diseaseadjuncts to
DMARD treatment
- Sering timbulkan GI discomfort ( dispepsia )
Obat :
- Aspirin (jrg digunakan), COX-2 inhibitors; non aspirin
NSAID mis: gol asam propionate (ketoprofen, ibuprofen),
gol as.asetat (diklofenak, ketorolak), oxicam (piroxicam),
COX-2 inhibitor (celecoxib)

- Tdk ada perbedaan efikasi

- Piroksikam timbulkan PUD dan GI bleeding

- NSAID lain spt celecoxib ,dosis tinggi ibuprofen dan


diklofenac  picu myocard infark
-ESO
* Dispepsia, komplikasi GI serius , ARF
-Faktor resiko induce ulser GI :
*usia > 60 th, rwyt ulser, obat (kortikosteroid,
NSAID dosis tinggi, anticoagulan,NSAID > 1
bersamaan)
-Monitor ketat px dg HF, peny liver dg ascites,
compromised renal function , diuretik scr bersa-
maan
- Data lab yg diperiksa : Cr, LFT tiap minggu
 NSAID baru
- Nitric oxide NSAID (COX inhibiting nitric oxide donors)
Mendonasi NO ke mukosa gaster, nitric oxide-NSAID
produksi efek gastoprotektif spt PG
- Hambatan jalur enzymatic metabolisme asam arakhidonat
(COX, 5-lypoxygenase)
- Aman pd sal cerna

 Vaksin RA
- induces a specific immune response against T cells
- masih trial fase II
 Corticosteroids
-antiinflammatory and immunosuppressive

- Interfere with antigen presentation to T lymphocytes,


inhibit PG and leukotriene synthesis, inhibit neutrophil
and monocyte superoxide radical generation

- Impair cell migration and cause redistribution of


monocytes, lymphocytes, and neutrophils  blunting the
inflammatory and autoimmune responses
- combination with DMARD → to improve clinical outcomes
(signs and symptoms, functionality,radiological damage)

- Long-term use of corticosteroids → serious adverse


effects (e.g., osteoporosis, weight gain, diabetes, cataract
formation, adrenal suppression, hypertension, infections,
impaired wound healing)

- Dose : oral corticosteroid with daily doses of 7.5 to 10


mg of prednisone (or equivalent), as short a time as
possible

- Frequent corticosteroid injections → to accelerate bone


and cartilage deterioration →the same joint should not be
injected more than once every 3 months
~ bridging therapy  used to control pain and
synovitis while DMARDs are taking effect

~ Alternate-day dosing of low-dose oral cortico-


steroids ineffective in RA ( symptoms usually
flare on days without medication )

~ High dose corticosteroid bursts are used to


suppress disease flares
~ High doses are sustained for several days until
symptoms are controlledfollowed by a taper to
the lowest effective dose
-Pemakaian alternate days trnkan resiko supresi
hypothalamic-pituitary-axis dg allowing kel adrenal
berrespon thd mediator hypothalamic & pituitary
-Pemakaian long term : osteoporosis
-Penamb suplemen Ca (1000 mg/hari), vit D (800
IU/hari), bntk aktif vit D (calcitriol ) cgh bone loss
pd px dg kortiko ≥ 5 mg/hari.
- biphosponat efektif cegah & tx kortiko induce bone
loss
- kortiko intra-artikular utk flaring occurs pd satu atau
few joint triamcinolone acetonide, triamcinolone
hexacetonide
- Bila efektif, injeksi i.a dpt diulangi tiap 3 bln

- Sendi yg sama tdk boleh diinjeksi > 2-3 x per


tahun  percepat joint destruction and atrophy of
tendons

- Dosis tunggal pagi hari menutupi sekresi kortisol


secara fisiologis dan minimalkan supresi hypotha-
lamic-pituitary-axis.
 Alkyllating cytotoxic agent
- Cyclophosphamide, chlorambucil : efektif utk RA
severe, resiko toksisitas (malignancy, infeksi)
* ESO : haemorrhagic cystitis

- Pd RA progresif yg tdk berrespon dg tx konservatif,


komplikasi RA yg ancam jiwa (rheumatoid vasculitis)
Terapi lain
- Minocyclin
*Terapi adjunctive RA yg disebabkan oleh infeksi.
- Cyclosporine
* efektif sendirian atau kombinasi dg MTX
* ESO serius : dose related renal toxicity, HT
• Pd refractory RA

• Dosis : 100–200 mg daily


 Monitor
- Efektivitas terapi
* Duration and intensity of morning stiffness
* Number of painful or tender joints
* Number of swollen joints; severity of joint
swelling
* Time to onset of fatigue
* ESR or CRP,Anti-CCP
* Radiographic changes: osteopenia, joint space
narrowing, bony erosions
2. CKD
- Problema medik pemakaian NSAID pada penyakit RA
dgn CKD identik dgn OA
- Methotrexate menyebabkan renal disfunction → kenaikan
Cr dan BUN , penurunan vol. urin ( dosis tinggi, presipitasi
obat)
- Penyesuaian dosis MTX perlu dilakukan pd CKD
* Clcr 10-50 ml/mnt : turunkan dosis ad 30-50%
* ClCr < 10 ml/mnt : avoid use
* pada HD , PD : tdk terdialisa, tdk perlu penambahan
dosis
- Pada chloroquin : - Clcr < 10 ml/mnt: turunkan dosis 50%.
- Terdialisis minimal
- Sulfasalazine : Clcr 10-30 ml/mnt : 2x1
Clcr < 10 ml/mnt : once daily
- Metilprednisolon dpt meningkatkan TD, retensi Na yg dpt
tingkatkan progresivitas renal disease
- Azathioprine : Clcr 10-50 ml/mnt : 75% dr dosis lazim

Clcr < 10 ml/mnt : 50% dr dosis lazim


- Cyclophosphamide : menyebabkan SIADH ( dosis > 50
mg/kg), renal tubular necrosis
* Clcr : < 10 ml/mnt : gunakan 75% dr dosis lazim
* terdialisis moderat ( 20-50%), perlu penambahan dosis
- Monitor : kadar Cr, BUN ( tiap 3 hari) , vol urin, TD,-
oedema
 Hepatic cirrhosis / hepatic impairment
- Pemberian NSAID akan meretensi Na ( perberat asci -
tes ) dan picu hematemesis melena
- Azathioprine bisa sebabkan hepatotoxicity
- Methotrexate akan sebabkan cirrhosis & portal fibrosis
( jk lama ), peningkatan akut liver enzyme ( dosis besar )
- Sulfasalazine : avoid use
- Kortikosteroid : ulcerative esophagitis, picu gastric
bleeding

- Monitor : BB, warna faeses, ALT, AST


 Diabetes mellitus
- Penggunaan kortikosteroid akan perparah hi-
perglikemia ( hambat sekresi insulin )
- Pemberian insulin perlu dilakukan ( back up )

- Monitor ketat kadar glukosa darah


 Cardiovascular disease (hypertension, HF)
- Penggunaan NSAID akan meretensi Na, hambat prosta-
glandin →tingkatkan TD, perburuk HF
- Cyclophosphamide akan perberat HF

- Chloroquin bs sebabkan cardiomyopathy ( fre-


quency not defined), aritmia
- Kortikosteroid ( t.u sediaan injeksi) → retensi Na →
tingkatkan TD, edema
- Monitor ketat : TD, edema, profil ECG
 Peptic ulcer disease / Melena
- Pemasalahan pemakaian NSAID pd pasien RA dgn PUD
~ OA
- Kortikosteroid : perparah PUD terkait hambat PG
- Methotrexate : sebabkan perforasi intestinal
- Perlu pemberian profilaksis stress ulcer
- Monitor : GI discomfort, gastric bleeding ( warna faeses )
 Hematologic disorder
- Penggunaan NSAID menyebabkan anemia, trombosito-
penia
- Azathioprine : bleeding, trombositopenia, leukopenia,
pansitopenia terkait efek myelosupressive
- Chloroquine : anemia aplastik, trombositopenia, neutro-
penia
- Cyclophosphamide : trombositopenia, anemia
- Methotrexate : leukopenia, trombositopenia
- Monitor secara ketat leukosit, trombosit, Hb, eritrosit
 Infection
- Penggunaan obat imunosupressan ( t.u
kortikosteroid ) dpt menekan sistem imun → picu
infeksi
- Dosis yg digunakan sekecil mgkn dan jk pendek
bila memungkinkan
 Marrietal status
- Pemberian imunosupresive drug pd pasien RA
sering menimbulkan problema fertilitas
- Cyclophosphamide : menyebabkan infertilitas
( ganggu oogenesis & spermatogenesis,
irreversible, supresi gonad ( amenorrhea)
- Methotrexate : defective oogenesis / spermato-
genesis
- Sulfasalazine : oligosperma ( reversible)
 Asessement
 Drug related problem
1. Ketidakcukupan regimen obat dlm penanganan nyeri
dan inflamasi, bisa disebabkan :
- terlambatnya manajemen awal terapi obat  kombinasi
DMARD ( dlm 3 bln)
- dosis dan frekuensi obat subterapeutik
- lama terapi yg kurang
- unresponsive therapy

 Rekomendasi
- Tingkatkan dosis dan frekuensinya
- Penggantian atau kombinasi obat DMARD ( 2 atau 3
obat)
 Monitoring
- Data klinik : -outcome nyeri dan inflamasi sekitar lokasi
-ESO : gastritis, perdarahan lambung
(warna BAB), nyeri kepala,
hemorrhagic cystitis

2. Drug induce
- Bisa berupa :
gangguan hematologi (anemia, trombositopenia,
leukositosis, leukopenia)
gastric bleeding
gastritis
aritmia
Drug induce hyperglikemia
DILI peningkatan ALT, bilirubin > 3 x nilai baseline
Drug induce kidney diseaseBUN dan Cr  (  30%)
Drug induce hipertensi
 Rekomendasi
- Stop dan / atau ganti obat yg dicurigai dgn obat yg lbh
aman
- Pemberian obat utk mengatasi drug induce
- Turunkan dosis obat ( dechallenge)
- Ubah rute obat ( oral suppositoria)

 Monitoring ketat
- Data klinik : TD, warna BAB, abdominal discomfort,
nyeri, inflamasi
- Data lab : nilai ALT/ALP, bilirubin, Cr serum, BUN, Hb,
trombosit, leukosit, glukosa drh
3. Ketidaktepatan dlm pemilihan obat, terkait dgn :
- Usia pasien : elderly fgs organ turun

- Penyakit komorbid ( CKD, CH, HT, HF, DM)  percepat


progresivitas penyakit
- Marrietal status → blm nikah

 Rekomendasi
- Stop dan / atau ganti obat yg aman utk elderly

- Ganti dgn obat yg tdk timbulkan fertilitas

- Penurunan dosis obat


- Pilih obat yg tdk KI dgn penyakit komorbid bila tdk bs
dihindari, monitoring ketat dan bila perlu diberikan terapi
tambahan ( back up therapy)
 Monitoring ketat
- Data klinik : ESO ( rash, erythema, SJS dll ), TD,
perdarahan lambung, nyeri, inflamasi
- Data lab : Cr, BUN,ALT/ASP,bilirubin, Hb, gluko-
sa drh
STUDI KASUS
1. Pasien an Ny. P, datang ke poli rheumatologi dengan
keluhan kekakuan sendi pada tempurung kaki tiap pagi
hari ± 45 menit, juga alami nyeri sendi. Dari anamnesis
dan data lab, terdiagnosis rheumatik artritis. Pasien
mendapat terapi obat Na diklofenak 3 x 50 mg,
prednison 3x 10 mg, kloroquin 250 mg 2 x 1. Pasien
juga menderita hipertensi dan CKD, berobat rutin ke poli
ginjal dan hipertensi. Data klinik pasien TD 160/100
mmHg, BB 55 kg,sedikit oedema. Data lab pasien Cr 4,5
g/dL ,BUN 78 g/dL, Hb 9,0 g/dL, RF (+)
2. Pasien a.n Tn G, MRS ke bangsal melati tgl 1 Oktober
2010 dgn keluhan panas selama 1 minggu, mual dan
muntah, bila BAK terasa panas dan nyeri. Pasien juga
alami nyeri pada pergelangan tangan dan kaki yang
sangat. Dari pemeriksaan, klinisi mendiagnosis ISK +
RA. Pasien mendapat terapi ciprofloxacin inj 2x200 mg,
pamol 4 x 1, antasida sir 3 x C II, lansoprasole 1 x 40
mg. Riwayat obat sebelumnya Ibuprofen 2x100 mg,
kloroquin 1 x 250 mg, metilprednisolon 3 x 4 mg. Data
lab SGOT / SGPT 100 U/L / 300 U/L, Cr 2,5 g/dL, BUN
50 g/dL
3. Pasien a.n Tn. S, usia 44 thn, Mrs dengan keluhan
tangan kanan mengalami kemerahan dan nyeri. Pasien
sebe-lumnya dirawat di Puskesmas, mendapat terapi
NaCl infus, ampisillin inj 3 x 1 g, punya riwayat RA dgn
mengkonsumsi methotrexate 2 x 2,5 mg, chlorokuin 2 x
250 mg, metil prednisolon 3 x 4 mg. Diagnosis pasien
selulitis. Data klinik : suhu 36 ○ C, TD 120 / 80 mmHg,
RR 20 x/mnt, Nadi 85 x/mnt. Data lab : leukosit 5500 /
mm3, Hb 11,5 g/dL, GDA 260 mg/dL, Cr 3,4 g/dL.-
Terapi yang didapat cefoperazon 3 x 1 g , Infus NaCl 0,9
% 15 tts/mnt, Actrapid 3 x 6 unit.
Bagaimanakah pharm care pada penyakit di atas ?