Ulcerative colitis

Ulcerative colitis
 Penyakit inflamasi immune-mediated kronis yang seringnya berlokasi pada rectum bersifat
difuse dan continue yg menyebar secara proksimal ke bagian usus besar. Hanya 5% UC yg
tidak melibatkan rectum, terutama onset masa kanak-kanak.
 UC banyak terjadi pada usia 15 dan 30 tahun

Faktor resiko (IBD)

 Usia 20-35 tahun
 White population
 Northern Europeans
 Yahudi
 Sosioekonomi tinggi
 Bukan perokok
 Pemakai kontrasepsi oral
 Diet rendah serat
Epidemiologi

Sumber: Harrison
 Pathophysiologi of UC
 Inflamasi terjadi pada recto-sigmoid area (proctitis)  extand left side of
colon  transverse colon( extensive)

 Genes & environmental  antigen sampling lewat m cell  translocation of

microbial product  aktivasi antigen-antibody reaction  CD4 T-cell
activation
1. CD4 T cell  aktivasi makrofag  produce cytokine, TNF alpha, IL-2, IL-6 
chemical inflammation  local systemic complication
2. TNF alpha  stimulasi angionenesis, paneth cell necrosis, IEC death and
impared barrier function, increase immune response, secret protese
(miofibrile induce dectruction)
“Cardinal sing”

 BAB berdarah (hematocezia)

 Urgency
 Tenesmus (nyeri setelah BAB)
 Abdominal cramps
 Weight loss
Systemic effect
 Ekstraintestinal manifestation  bacteri yg lolos lewat damage mucosal
layer,induce immune response, body can’t discriminate them

- dermatologic - erythema nodosum, pyoderma gangrenosum, oral aphthous

ulcers
- rheumatologic - peripheral arthritis, ankylosing spondylitis
- ocular - conjunctivitis, uveitis/iritis, episcleritis
- hepatobiliary - steatosis, PSC
- urologic - calculi, ureteral obstruction, fistulas
- metabolic bone disorders - low bone mass

Clinical approach

1 Anamnesis : how to differentiate remission & excacerbation of the diseases

2 Physical examination : abdominal cramp, weight loss, extraintestinal mani-

festation

3 Laboratorium : LED, CRP, stool examination

4 Endoscopy, Radiology, pathology anatomy

5 Therapy evaluation
Anamnesis

Stomatitis
Suspek psoriasis
Arthritis
Derajat UC

To indentify acute severe UC

Acute severe UC

 Should have stool testing  rule out CDI

 Undergoing flexible sigmoidoscopy within 72 hours  evaluate CMV colitis
 Assest for toxic megacolon, colonic perforarion, severe refractory bleeding 
surgery indication
 Monitor therapy respons : stool frequency, rectal bleeding, physical
examination, vital sign, serial CRP
 Avoid anticholinergic side effects
 Failed therapy 3-5 days  consider surgery
Severity of UC after diagnosed
Diagnosis

 Feses rutin rule out clostridiodis difficile

 Serology testing  diagnostic dan prognosis
 Endoscopy
 Biopsy
UCEIS
Pathology

Macroscopic features:
 Microscopic features
 Mild inflammation : mucosal
erythema, granular surface like
sandpaper
 Severe inflammation : mucosal
haemorrhage, ulcerated,
edematous
 Long standing-disease : featureless
& anthropic mucosal, narrowed
lumen & shortend
 Fulminant disease : megacolon, can
be perforated
Based on AGA guideline
Therapy recommendation

 Mild procitis  rectal 5-ASA dose 1g/d

 Mild left-sided  rectal 5-ASA enemas dose 1 g/d or 5-ASA enemas + oral 5-
ASA dose 2 g/d , if intolerate or non responsive choose oral budesonide multi-
matrix(MMX) dose 9mg/d
 Extensive UC  oral 5-ASA dose 2g/d, if non responsive choose oral systemic
corticosteroid

Sumber AGA guideline

Therapy cont’

Sumber: Harrison
 SCCAI

Index aktivitas penyakit

Prognosis
5-AMINOSALICYLATE

 Sulfasalazine : azo-bond prodrug, mesalazine disintesis lalu berikatan dengan

azo-bond, tdk diabsorpsi di upper GI -> di colon azo-bond dipecah oleh
azoreductase  active component of mesalazine
SE : anemia, abnormal liver enzyme  prevensi, asam folat 1 mg/day
 Mesalamine
 Mild-moderate UC : start oral 5-ASA 4.8 g/day for induction remission , tap off
2.4g/day  if remission no achieve, use combination with topical 5-ASA