Pandji Mulyono,MD,Internist

Gatot Sugiharto, MD, Internist

Faculty of Medicine, UWKS
Lecture - 2011
Kapita selekta
Dyspepsia
Epigastric fullness, discomfort, vague term (indigestion)
Dysphagia
Difficulty swallowing, feeling of food sticking in oesophagus
Odynophagia
Painful swallowing usually associated with dysphagia
Heartburn
Burning sensation retrosternally associated with reflux
Anorexia
Loss of appetite
Haematemesis
Vomiting blood (could be red or altered coffee ground)
Melena
Passing of black tarry, offensive stool (usually due to upper GI bleeding)
Haematochezia
Passing blood per rectum (PR bleeding)
PENYAKIT GI PERLU AX TELITI

O Keluhan GI dapat berkaitan gangguan :
Lokal /Intralumen :
O Gastritis
O Dounenitis dsb
Sistemik
O Gastropanese Diabetikorum

Sakit perut ini dgn Ax, Px yang baik akan dapat dijabarkan apakah
sakitnya :
Nyeri epigastrik
Kolik bilier
Kolik usus
Nyeri akibat rangsangan peritorial


DISPEPSIA
O Sindroma : nyeri /tidak nyaman di ulu hati . Kembung , mual ,
muntah, sendawa, rasa cepat kenyang, perut rasa penuh
/begah (sangat variatif bagi penderita)
O Maka cari etiologi Dipepsia :
Dalam lumen saluran cerna
OTukak gater /duodenum, gastritis, tumor, infeksi H pylori
Obat-obatan
ONSAID, Aspirin, Digitalis, teofilin, beberapa antibiotik
Penyakit (organ)
OHati, pankreas, sistem bilier

CONT
O Penyakit sistemik
DM, Tirotoksikosis, PJK
O Bersifat fungsional :
Tidak ditemukan gangguan organik / struktur/biokimia
disebut juga Dispepsia fungsional / non ulkus
PENDEKATAN DIAGNOSTIK
Ax : sifat lokal / sistemik dst
Px : tumor, organomegali,
nyeri tekan dst
Lab :
Infeksi ? Lekositosis
Pankreatitis Amilase, Lipase
Keganasan CEA, AFP, CA 19-9 dst
CONT
OUltrasonografi
OEndoskopi.dianjurkan bila +alarm simtom
OFoto UGI

OAlarm Symptom :
Anemia, berat badan turun, hematemesis,
melena, lama, usia > 45 tahun
disfagia
Suatu gangguan psase Makanan dari mulut ke lambung

Disfagia
Fase
orofaringeal
Gejala : regusgitasi ke hidung,
terbatuk batuk waktu berusaha
menelan/waktu menelan
Etiologi : CVA , miastenia gravis kelainan
muskuler,tumor,divertikulum
zenker,gangguan motilitas/spinter
esofagus atas
Fase esofageal
Gejala : mampu telan ttp yg ditelan
terasa tetap mengganjal/tdk mau
turun disertai nyeri etrosternal
Etiologi : inflamasi , striktura
esofagus, tumor,penekanan dari
luar esofagus, akalasia spasme
esofagus defus, skleroderma
ODINOFAGIA
O Rasa sakit waktu menelan

O Pendekatan diagnostik
Esofago gastroskopi
Barium meal ( esofago grafi)
Manometri esofagus
GERD (GASTRO ESOPHAGEAL REFLUX
DISEASE)
OSuatu keadaan patologis akibat refluks kandungan
lambung, melibatkan :
1. Esofagus
2. Faring
3. Laring
4. Saluran nafas

Akibatnya memberi gejala dalam maupun luar
esofagus
REFLUX PADA GERD MELALUI 3 MEKANISME
1. Reflluks spontan saat melaksanakan LES yang
tidak adequat
2. Aliran retrogard yang mendahului kembalinya
tonus LES setelah menelan
3. Meningkatnya tekanan intra abdomen

LES : Low Esofagus Spincter
PATOGENESA TERJADINYA GERD
Pemisah Anti reflux me
nyangkut keseimbangan
Faktor defensfif
osefagus ~
LES yg ok

1.Hiatus hernia
2. Panjang LES
3.Obat-obatan antikolinergik; beta
adrenergik,teofilin,opict
4.Progresteron (wnt hamil) meningkat
ofensif bahan
refluksat
HCl
Pepsin
Empedu
Enzim2 Pankreatik
OBersihan asam dari Lumen esofagus tergantung
faktor gravitasi,
peristaltik,
ekskresi air liur dan bikarbonat
OKetahanan epitel esofagus, tidak memiliki lapisan
mukus untuk lindungi mukosa seperti gaster
/duodenum
MANIFESTASI KLINIK
ONyeri /rasa tidak enak dari epigastrium atau
metrosternal bagian bawah (seperti
terbakar/heartburn), kadang-kadang dengan
disfagia, mual, rasa pahit di lidah.
O Kadang kadang timbul gejala ekstra esofagus;
nyeri dada non kardiak, suara serak, laringitis,
batuk-batuk karena aspirasi.
DIAGNOSIS
1. Endoskopi
2. Esofagografi dengan barium
3. Pemantauan Ph 24 jam
4. Manometri esofagus
5. Tes Bernstein
6. Sintografi gastro esofagraf
7. PPI test


Slang tran nasal sp distal
esofgus dgn Hcl 0,1 M kurang
dari 1 jam nyeri
(dibandingkan dgn N Cl tdk
menimbulkan nyeri)
Radio isotop dalam
makanan
PPI dosis tinggi 1-2 minggu
+ bila ada perbaikan 50%-
75% gejala

PENATA LAKSANAAN GERD


O Pada dasarnya Tx GERD;
Modifikasi gaya hidup

O Medikamentosa

Pembedahan

Tx Endoskopik
PENATALAKSANAAN
O Modifikasi gaya hidup
1. Cara tidur ; tidak makan sebelum tidur
2. rokok, alkohol ( LES, epitel)
3. Konsumsi lemak dikurangi, kalori ; karena distensi
lambung
4. Turunkan BB, pakaian ketat
5. Hindari coklat, teh, kopi, soda, pepermint, OK stimulasi
asam
6. Hindari obat-obatan turunkan LES
TERAPI MEDIKAMENTOSA



O Terapi supresi asam lebih unggul
dp prokinetik

1 PPI mrpk pilihan utama
hasil 80 % dlm 6-8 mgg
maintenance bila perlu

2 ANTASIDA
Bufer thd asam hcl dan perkuat LES
CONT
O Efektip dan aman dlm hilangkan simtom
O ttp tdk sembuhkan lesi
O rasa kurang enak dpt timbul diare (Mg) konti
pasi(Alluminium) hati2 pt dgn ggn ginjal



CONT
O 3. Antagonis-reseptor H2
(simitidine ranetidin ,famotidine,nizatidine)

O 4 Obat prokinetik;
Teoritis paling sesuai untk GERD (dianggap ggn
motilitas) ttp praktisnya tgt penekanan asamnya
Metoklopramid;
dosis 3x 10 mg
bisa lalui sawar darah otak
____> mengantuk,
pusing agitasi tremor ,diskinesia

DOMPERIDON
O Meningkatkan tonus LES dan percepat
O pengosongan lambung
CONT
O 5.Sukralfat(aluminiumhidrksida +sukrosa okta sulfat)

Bekerjasecara Topikal(sitoprotektip),meningkatkan
pertahanan mukosa,sbg buferthp hcl serta dpt mengikat
pepsin dan garam empedu
TERAPI THDP KOMPLIKASI GERD
O Stritura ,perdarahan,Barretts esofagus resiko
ke Ca 30-40 kali populasi normal
O Pada stiktura esofagus;bila diameter < 13 mm dpt
dilakukan dilatasi busi ( Maloney bougie,Hurst bila
gagal operasi)
O Tx bedah bila gagal medikamentosa dan resiko CA
ESOPHAGITIS

O Etiology : infection or irritation
Infection : bacteria, viruses (herpes), fungi, and yeast
(Candida)
Irritation : primary or secondary to gastroesophageal reflux,
hiatal hernia, vomiting, surgery, medications, Lye, Radiation
O Symptoms: Dysphagia, Odynophagia, Heart Burn
(reflux), oral lesions (herpes)
O Tests : Barium esophagogram, acid perfusion tests
(Bernstein), culture, Esophagoscopy (gold standard)
O Treatment depends on the specific cause
O Complications: severe discomfort, swallowing difficulty,
malnutrition /dehydration, scarring, Barrett's esophagus,
cancer

BARRETTS ESOPHAGUS
O Esophageal squamous epithelium replaced with
metaplastic columnar epithelium
O Incidence up to 10%/lifetime
Usually men >55
GERD commonly present
O Dx : esophagoscopywith biopsy
O Treatment:
Treat reflux aggressively PPI
Surveillance for dysplasia
O No dysplasia q 3-5 years
O Dysplasia confirm with expert pathologist/
GI specialist

ACHALSIA
A diffuse motor disorder: incomplete relaxation of the
L.O.S and absence of peristalsis (cardinal finding to
make a diagnosis)
Symptoms: dysphagia, regurgitation, and the classic
x-ray finding of gradual tapering of distal esophagus
(birds beak)
Esophageal manometry (gold standard)
Treatment
Esophageal dilatation
Surgery
Botulinum toxin injections into L.E.S
SWALLOWING DISORDERS :
DYSPHAGIA
O Common in aging persons > 50 years
O Oropharyngeal dysphagia : dysfunctional transfer from pharynx
to esophagus (Stroke is the leading cause)
O Esophageal dysphagia: disordered peristaltic
motility(Neuromuscular Disorder) or (Mechanical Obstruction)
Differential Diagnoses
Mechanical obstruction : benign stricture (burn injury, web, GERD),
malignant obstruction (SCC, Adenocarcinoma)
Neurological : CVA, achalasia, MND, Myaesthenia Gravis, Parkinsons
Functional
Management
Diagnosis specific and multifactorial


ODYNOPHAGIA
A strong feeling of burning, squeezing pain while
swallowing or chest pain, food stuck in the throat, or
heaviness or pressure in the neck or upper chest
Mechanism : destruction of the mucous membrane,
infection, chemicals, or motor disorders of the
esophagus
O Can be associated with many of the disorders that
cause dysphagia
O Common causes : Infection, abscess, gum disease,
pharyngitis, Thrush (Candidiasis), HSV, CMV, HIV,
Ulcers Esophagitis
O Rarely, a foreign body, Esophageal motor disorders,
such as achalasia
UPPER GI BLEEDING
O Manifestation :
Hematemesis and/or melena (black tarry
stools)
Hematochezia (maroon or bright red blood per
rectum) when massive
O Diagnosis-clinical presentation : NG lavage
O Risk factors : Aspirin or NSAID use (most
common cause), Helicobacter Pylori infection,
Elderly (especially over age 70 years)

COMMON CAUSES OF BLEEDING IN
THE DIGESTIVE TRACT

Esophagus
Inflammation
(esophagitis)
Enlarged veins
(varices)
tear (Mallory-Weiss
syndrome)
Cancer
Stomach
Peptic ulcers
Inflammation (gastritis)
Cancer

Small Intestine
Duodenal ulcer
Inflammation
(inflammatory bowel
disease)
Angiodysplasia
Large Intestine and
Rectum
Hemorrhoids
Infections
Inflammation (IBD)
Colorectal polyps
Colorectal cancer
Diverticular disease

UPPER GI BLEEDING
(1)

O Mechanism
Inflammatory: peptic ulcer, esophagitis, gastritis, stress ulcer, duodenal
ulcer, inflammatory bowel dz
Mechanical:mallory-weiss tear, hiatal hernia
Vascular: esophageal varices
Neoplastic: carcinoma
Systemic: blood dyscrasias
O Causes: Duodenal Ulcer (30-37%) , Gastric Ulcer (19-24%),
Esophageal Varices (6-10%), Gastritis or Duodenitis (5-10%),
Esophagitis or esophageal ulcer (5-10%), Mallory-Weiss tear (3-7%),
Gastrointestinal malignancy (1-4%), Dieulafoy's Lesion (1%),
Arteriovenous malformation , Angiodysplasia of stomach or duodenum,
Chronic Renal Failure, Cirrhosis, von Willebrand's Disease

UPPER GI BLEEDING
(2)

Management
O Endoscopic treatment
Thermal coagulation (heater probe, gold probe, BICAP)
Injective sclerotherapy (epinephrine)
Combination therapy commonly used for high risk causes i.e. active
bleeding
Endoclips
O Antisecretory therapy
PPI : Omeprazole i.v. decreases rebleeding after endoscopic treatment
H
2
blockers disappointing results
Octreotide (somatostatin analoque) reduce rebleeding
O 50-100 mcg bolus, 25-50 mcq/hr for up to 3 days
O Surgery


GASTRITIS (Patofisiologi)
ADALAH :
PROSES INFLAMASI MUKOSA LAMBUNG,
YANG DAPAT :
a. MENGENAI MUKOSA LOKAL/DIFUS
b. BERLANGSUNG AKUT/KRONIK.
ETIOLOGI / PATOGENESIS :

FAKT. AGRESIF FAKT. DEFENSIF
- GASTRIC ACID - MUCOUS
- PEPSIN - BIKARBONAT
- BILE REFLUX - PROSTAGLANDIN
- NSAID - PHOSPOLIPID
- CORTICOSTEROID - EPITHELIAL CELL
- ALKOHOL - MUCOUS BLOOD FLOW
- NICOTINE - MOTILITY
- H. PILORI
PENATALAKSANAAN :
1. ANTASIDA
2. H
2
BLOCKER / PPI.
3. ANTI KOLINERGIK ?
4. SITOPROTEKTIF :
A. SISTEMIK : PROSTAGLANDIN :
MISOPROSTOL, ENPROSTIL.
B. LOKAL :
SUKRALFAT,
KOL. BISMUTH SUBSITRAT.
PENATALAKSANAAN :
1. ANTASIDA
2. H
2
BLOCKER / PPI.
3. ANTI KOLINERGIK ?
4. SITOPROTEKTIF :
A. SISTEMIK : PROSTAGLANDIN :
MISOPROSTOL, ENPROSTIL.
B. LOKAL :
SUKRALFAT,
KOL. BISMUTH SUBSITRAT.
Peptic Ulcer Disease
Ulceration caused by acid/pepsin
Stomach, Oesophagus, Duodenum, Meckels diverticle
Symptoms
Often none
Gnawing abdo pain (epigastric)
Vomiting/nausea
E Aetiology
Helicobacter pylori
Up to 90% of DU and 75% of GU
NSAIDs (Non steroidal antiinflammatory drugs)
Physiological stress

TUKAK GASTER
Definisi
suatu gambaran bulat/oval ukuran> 5 mm kedalaman
submukosa pd mukosa lambung
akibat terputusnya kontuinitas/integritas
mukosa lambung

Etiologi
utama; HP,dan OAINS
jarang;sdrma Zollinger Ellison ,Crohn douden,

Patofilogi tukak peptik
E Schwarst 1910;No acid no ulcer
E Balance Teori 1974; tukak terjadi bila ggn
keseimbangan f agresip dan f defensip
E Sel parietal(oksintik) sekresi hcl,sel zimogen sekresi
pepsinogen kena hcl jadi pepsin mrpk f agresip
merusak barier mukosa ,histamin keluar merangsang
untk lebih banyak mengeluarkan asam lambung,terjadi
dilatasi
E Dan peningkatan permiabilitas kapiler ----
E -- kerusakan mukosa lambung,gastritis akut/kronik
dan tukak gaster

Gambaran klinis
Umumnya keluhan dispepsi(4 mcm dispepsi)
1 akibat ggn motilitas; kembung,kenyang disertai
sendawa,rasa penuh ulu hati sth makan
2 akibat refluk; nyeri ulu hati ,rasa tdk nyaman dan muntah
3 akibat tukak nyeri ulu hati, rasa tdk nyaman dan muntah
4 tak spesifik;
dispepsia non tukak juga timbulkan sakit yg sama,lokasi
tdk jelas tukak akibat OAINS tukak pd manula biasanya
tdk timbulkan keluhan ttp
komplikasinya perdarahan/perforasi

Cont
E Pada tukak doudeni;
E rasa sakit timbul wkt pt merasa lapar,rasa
sakit hilang stlh makan dan minum antasid
(HPFR= Hunger Pain Food Relief) dan letak
nyeri sblh kanan garis tengah perutbeda

+ Pada tukak gaster; rasa sakit sebelah kiri,rasa sakit
stlh makan. Bisa menjalar ke punggung,tanda
tambah erat/penetrasi ke pankreas
Pemeriksaan fisik
Tukak tanpa komplikasi fisik taa,paling nyeri ulu
hati
O Penurunan BB
O Bila ada retensi cairan --stenosis pilurus

Pemeriksaan penunjang
O Barium meal/UGI FOTO
O Endoskopi
Diagnosis
+ Klinis--- dispepsia dsb apa lagi ada sugesti
pt tukak (Ax kluarga,OAINS,rokok ,alkohol
HP + )

+ Penunjang (UGI/Endoskopi )

+ Biopsi,histologi HA
DD
O Dispepsia non tukak/ fungsional
O GERD
O Tumor
O Penyakit vaskulitis
O Penyakit pankreo bilier
O Gastrodudenal Cronhs disease
Komplikasi tukak
+ Perdarahan

+ Perforasi/penetrasi

+ Obstruksi/stenosis
Terapi
E Non medikantosa

E Medikantosa

E Tindakan
PENGOBATAN MEDIK
1. MERINGANKAN/MENGHILANGKAN KELUHAN
2. KESEMBUHAN TUKAK
3. MENCEGAH TERJADINYA KOMPLIKASI
4. MENCEGAH TERJADINYA KEKAMBUHAN

ERADIKASI KUMAN H.p :
SULIT, O.K KUMAN H.p DIBAWAH LAPISAN MUKOSA.
ERADIKASI DICAPAI SETELAH > 4 MINGGU PENG-
OBATAN DG ANTI MIKROBA ATAU H.p (-).

ADA 3 KATEGORI TERAPI H.p :
1. BIS TRIPLE : (BIS TET MET)
2. IPP TRIPLE : IPP CLA MET
IPP AMO CLA
IPP AMO MET
3. QUADRIPLE : IPP BIS TET MET

KONSENSUS (KSHPI : 1996) : TRIPLE SELAMA 2 MINGGU
PENYEBAB PA
E Alkohol,merokok diit lemak tinggi
E Batu empedu
E Toksin dan obat(azatioprin,pentamidin,furose
semid,captopril
o Metabolik faktor
TG > 1000mg(bila <200mg terhindar)
o Trauma (hipotensi/hipoperfusi) picu PA
ERCP < 5% picu PA
o Auto imun,virus,genetik
Manifestasi klinik
E KAS;
- nyeri epigastrium,nausea,vomiting nyeri ini
menjalar ke punggung bbrp jam tdk hilang walau
sdh muntah
- Px ;nyeri raba setempat/seluruh perut,
- distensi ikterus bisa ok batu/edem bila berat suara
usus hilang(ileusintestinal),hipotensi,
takikardi,takipneu,hipertermia
- Pada kulit indurasi daneritema ok subkutaneus
nekrosis,
Cont manifest
E Pada necrotising PA ;ekimosis luas di pinggang
dsbt GREY TURNER SIGN, dan area umbilikus
dsbt CULLEN SIGN ok blood dissecting
retro peritonial

Diagnosis

E Klinis
Labolatoris peningkatan
Amilase 212jm kemudian jadi normal 3-5 hari,tdk spesifik
ttp bila kenaikan.>3 kali

O MENUNJANG DIAGNOSE
Tetapi amilase naik pd obstruksi usus halus,infark, perforasi
duodenum ulcer, yg non gastro spt paru tuba falopii,kelenjar
ludah Lipase paralel dgn amilase lebih panjang.
Lekositosis,transiet hiperglikemi ,hiperbilirubin,alkalifosfatase
dsb
Pengelolaan Akut Pancreatitis
(

E Early ERCP for gallstone pancreatitis + elective
cholecystectomy
E Pain control Meperdine, Morphine or Fentanyl
E Prophylactic antibiotics : Imipenem,
fluoroquinolones
E Enteral Feeds : high protein, low fat
E Complication : Pseudocyst/abscess, hemorrhage due
to ulceration, hematoma, Shock, ARDS, ARF,
hyperglycemia and hypocalcemia

Chronic Pancreatitis
E Most common etiology alcohol
E Diagnosis based on clinical criteria in the setting or
recurrent abdominal pain assisting by imaging
Pain: epigastirc, radiates to back postprandial
Pancreatic insufficiency: 90% of pancreas usually destroyed.
Loose, greasy, foul smelling stools that are difficult to flush.
Diabetes is usually insulin requiring
Amylase/Lipase commonly normal
Imaging USG, CT Scan, MRI, ERCP, Endoscopic U.S.,
Plain films
Gambaran klinis
E Nyeri epigastrium sering menjalar ke punggung
E Diare,steatorea
E Distensi dan kembung
E Penurunan berat badan
E ikterus
Pengelolaan
O Edukasi
Diet,rendah lemak alkohol,bila DM ada sesuikan

O Medikamentosa;
+ analgetik,enzim pankreas tripanzim pankreoflat
+ OAD bila ada DM

O Tindakan;
penbedahan misal drinase ,reseksi,ERCP,
ESWL(Extracorporeal shoch waves)

Diare Adalah Defekasi
Cair Yang Frekuensi dan
Jumlahnya Meningkat.
Defined as watery or liquid stools, usually with
increases in daily frequency and in total stool weight
(>200 g per day)
More than 3 times per day, less than 14 days,
usually spontaneously resolves
Etiology : Bacterial, viral, parasitic, non-
infectious
Mechanism : impaired balance between resorption
and secretion in the intestinal wall which leads to
the increased wateriness of the feces


Causes of acute diarrhea
Non
inflamatory
diarrhea
Agent Inflamatory
diarrhea
Agent
Viral Norwalk virus, Norwalk like
virus, Rotavirus
Viral Cytomegalovirus
Protozoal Giardia lamblia,
Cryptosporidium
Protozoal Entamoeba hystolytica
Bacterial Preformed enterotoxin :
Staphylococcus aureus,
Bacillus cereus, Clostridium
perfringens
Bacterial Cytotoxin production :
Enterohemorrhagic E.coli (EHEC),
Vibrio parahemolity- cus,
Clostridium difficile
Enterotoxin production :
ETEC, Vibrio cholerae
Mucosal infection : Shigella,
Campylobacter jejuni, Salmo-
nella, Enteroinvasive E.coli (EIEC),
Aeromonas, Plesio-monas,
Yersinia enterocolica, Chlamydia,
Neisseria Go, Listeria
monocytogenes
Empirical AB (while awaiting culture) based on : Fecal leukocyte (+), Bloody diarrhea, abd pain, dehidration, >
stools/24h, immunocompromized, elderly
ACUTE DIARRHEA
DIFFERENTIAL DIAGNOSIS
Infectious-classical
Salmonella
Campylobacter
Shigella
Yersinia
Mycobacterium tuberculosis
Clostridium difficile
Escherichia coli
Entamoeba histolytica
Balantidium coli
Lamblia
Neisseria gonorrhoea
Treponema pallidum
Herpes simplex
Clamydia trachomatis
Viruses
Infectious-new
Histoplasma
Cytomegalic virus

Drug induced
Pseudomembraneous colitis
Contraceptive-induced colitis
NSAIDs-induced enteritis
invasive
toxic
parasitic
sexually
transmitted
Immuncompr.
(HIV)
PEMBAGIAN :
MENURUT PATOGENESISNYA :
1. PENGELUARAN CAIRAN USUS :
a. SEKRESI YANG BERLEBIHAN
AKIBAT PENGARUH TOKSIN : CHOLERA
b. PROSES RADANG : TERJADI EKSUDASI
MISAL : AMUBIASIS, SHIGELOSIS.

2. GANGGUAN ABSORPSI :
a. BAHAN OSMOTIK YANG TAK DISERAP : PENCAHAR
b. MOTILITAS USUS MENINGKAT : BAHAN IRITATIF
c. PERMUKAAN USUS BERKURANG : RADANG, RESEKSI.
MENURUT ONSETNYA :

1. AKUT
a. INFEKSI :
- BAKTERI : VIBRIO, SALMONELLA, E. COLI .
- VIRUS, JAMUR, PROTOZOA, CACING.
b. BAHAN TOKSIK :
- BAKTERI, BAHAN KIMIA.
c. MAKANAN :
BERSIFAT IRITATIF, ALKOHOL, ALERGI,
INTOLERANSI.

2. KRONIK :
KELAINAN DAPAT DI GASTER, DUODENUM, COLON.
TERSERING :
- FUNGSIONIL : IBS, EMOSI
- COLON : DIVERTIKULITIS, CARCINOMA, IBD.
- DUODENUM : SINDROMA MALABSORPSI.
- GASTROGENIK : POST GASTREKTOMI.
- PEMAKAIAN LAKSATIF.
UNTUK KEPENTINGAN KLINIK, DIBEDAKAN 2 BENTUK :
1. GASTROENTERITIS DISENTRIFORM :
O.K. : SHIGELLA, SALMONELLA, E. HISTOLITIKA.

2. GASTROENTERITIS CHOLERIFORM
O.K. : VIBRIO, E. COLI, CLOSTRIDIA, INTOKS. MAKANAN.
PENYEBAB UTAMA DEHIDRASI DAN SYOK
RARE CAUSES OF CHRONIC DIARRHEA
Post gastrectomy syndrome
Diabetic gastroenteropathy
Endocrine disorders hyperthyreoidism
hypothyreoidism
hyperparathyreoidism
hypoparathyreoidism
Addisons disease
Collagen disorders
Pernicious anemia
History / physical examination
Stool inspection
Laboratory (inflammation, anemia, special tests)
Microbiology (parasites)
Tests for absorption (breath tests, direct tests)
Endoscopy / histology
Radiology
DIAGNOSTIC TECHNIQUES
FOR DIARRHEA
With fever and blood (invasive pathogen)
inflammatory diarrhea
Shigella, Campylobacter, Salmonella
Leukocytes in feces, fecal culture(+)
Tx : Antimicrobials for persistent shigella,
salmonella or campylobacter infections
especially: immunocompromised px
No fever or blood (Non-invasive pathogens) non
inflammatory diarrhea
No leukocytes in feces, fecal culture (low yield)
Etiology :
Enterotoxic E.coli (ETEC) , Giardia, Rotavirus, Norwalk,
Parasites
Traveler's diarrhea (85% of cases)
Tx :
Correct dehydration, spontaneous recovery except treat
parasite infection
Most viral and bacterial causes of diarrhea resolve without
treatment, antibiotics may prolong or worsen diarrhea

Lasts for more than 2 weeks
Infectious: parasites, bacteria, viral
Non Infectious :drugs, crohns disease, endocrine diseases, food
additives (sorbitol, fructose, and others), food allergies, GI
surgery or radiation, tumors, intestinal ischemia, lactose,
caffeine, ethanol
Usually related to functional disorders like irritable bowel
syndrome (IBS), celiac disease, or inflammatory bowel disease
(IBD)
Endoscopy more specific than radiographic studies in diagnosis
the etiology

IBS: Abdominal pain associated with altered
stools (diarrhea or constipation), no organic
cause identifiable
Symptoms include
Bloating, flatus, mucous in stool
Exacerbated by stress
Diagnosis: Rome III criteria :
Recurrent Abdo pain for 3 days in the last 3 months with 2 of:
Improvement with defecation
Onset associated with change in stool frequency
Onset associated with change in stool form
DIFINISI
Adanya nyeri perut,distensi dan ggn pola
defekasi tanpa ggn organik
,Mengenai perempuan 3kl besar dp laki2

ETIOLOGI; ??
Multi faktor;ggn motilitas,intoleransi mknan
hipersensifitas ,paska infeksi,ggn senso
ris dsb
Dipakai kreteria Rome II;
Sedikitnya 12 mgg /> (tdk selalu berurutan)
selama 12 bln terakir dgn rasa nyeri/tdk
nyaman di abdomen disertaidgn adanya
2 dari 3hal berikut;
1 nyeri hilang dgn defekasi; dan atau
2 awal kejadian di hbkan dgn perubahan
frekuensi defekasi dan atau
3 awal kejadian dihbkan perubahan bentuk
feses.
Gejala lain yg mendukung IBS;
=frekwensi defekasi abnormal
=bentuk feses abnormal
=proses defekasi abnormal(tdk tuntas,ngejan)
=adanya mukus/lendir
=kembung/distensi abdomen
(Apakah nyeri yg diraskan pd satu tempat
apa pindah2? (pd IBS pindah2)
Seberapa sering merasa nyeri?
(pd IBS tdk tentu)
Brp lama nyerinya ?(pd IBS sebentar)
Bgmn nyerinya jika sudah defekasi/flatus?
(pd IBS lebih nyaman
Non medikamentosa
diet serat tinggi pd IBS konstipasi
diet rendah serat pd IBS tipe diare
kurangi bhn2 pencetus spt cafein susu gan
dum,bawng, coklat bbrp sayuran dsb
Olah raga
Edukasi tx psikoterapi

Obat2 an
anti spasmodik
laksatif
dll
Adalahpeny, inflamasi yg libatkan saluran cer
na dgn penyebat blm diketahui
Aetiology
Probable polygenic disease
Environmental (gut infection)
Immunological
Symptoms
Can be varied depending on site
Often: Diarrhea, abdominal pain, hematochezia, PR
mucous
Nutritional disorders
Iron deficiency, Vitamin B12 deficiency, Folate deficiency etc
Extraintestinal manifestations
Arthritis, Uveitis, Skin changes, Primary Sclerosing Cholangitis
Crohns Disease
Pathology throughout GI tract
Often skip lesions with intervening normal gut
Transmural inflammation and fistulous disease
Ulcerative Colitis
Localised to the colon and rectum
Mucosal inflammation characteristic
Usually contiguous disease
Occasionally difficult to distinguish the two
Indeterminate Colitis

Gambaran klinis pd Ulseratif colitis lebih
seragam,krn hanya colon saja yg terlibat,

pd Crohn d lebih bervariasi,krn melibatkan
semua saluran cerna (mulutanorektal)
adanya fistula(perianal)mrpk hal yg karak
teristik,nyeri perut lebih menyolok,


Medical
Nutritional replacement
Oral 5-aminosalicylates
Sulphasalazine, Mesalazine
Antibiotics
Corticosteroids (oral/IV)
Immunomodulators
Azathioprine, Methotrexate
Anti-TNF antibodies
Infliximab, Adalumimab



Surgical
Resection of bowel
Abscess drainage
Fistula
repair/strictureoplast
y (Crohns)
Less than three stools per week
Patophysiology : excess absorption of water + slow passage in
the colon
Possible causes : motility or pelvic floor disorder, endocrine
disorder
Older people : chronic illnesses, low fiber diet, neurologic and
psychiatric, medicines, immobility
In infancy and childhood : most is functional
Treatment : symptomatic
A lot of water, regular exercise, move bowels when urged, a
diet rich in fiber (30 - 35 grams daily)
Gentle enema, avoid stimulant laxatives


A. Melena. Passage of black, tarry stools secondary to GI bleeding
with intestinal transit time allowing for the digestion of
hemoglobin.
1. May be of upper or lower GI origin
2. Fals positive : ingested iron, licorice, or bismuth but the stool will
be guaiac negative.
A. Hematochezia. Bright red blood per rectum.
1. Can be secondary to anal disease (hemorrhoids, rectal fissure).
2. May be secondary to a bleeding diverticulum, other colonic
disease such as angiodysplasia, Crohns disease, ulcerative colitis,
carcinoma (very rarely causes gross bleeding), dysentery
(especially amebiasis, campylobacter, shigella, or other invasive
organisms).
3. Ingestion of beets may simulate hematochezia.


A. Laboratory studies : CBC and platelets, PT/PTT, electrolytes,
BUN/creatinine. Blood type and crossmatch for tranfusion
B. Physical examination : hyperactive bowel sounds, acute
abdomen
C. Radiology : CXR and an upright abdominal film to look for
free air.
D. Endoscopy (for upper GI bleeding) : define the source and
treat endoscopically
E. Angiography or nuclear medicine studies can be useful to
localize lower GI bleeding.

1. Fluid resuscitation and manage shock .
2. Urgent therapeutic colonoscopy with
epinephrine injection or bipolar coagulation in
patients with severe hematochezia and
diverticulosis.
3. A surgical consultation should be obtained in
case operative intervention is needed.

Occult : positive fecal blood test without visible blood
Source : more commonly from upper GI tract than in the
lower gastrointestinal
Investigation : colonoscopy and upper endoscopy
Obscure : bleeding of unknown origin that persists or recurs
after negative endoscopic evaluation
Investigation :
Radioisotope bleeding scans
Angiography : identify highly vascular nonbleeding lesions such as
angiodysplasia and neoplasms
Wireless capsule endoscopy for small bowel lesions

Most frequent causes of anorectal bleeding
are hemorrhoids, fissures and polyps
High index of suspicion for cancer
Evaluation of bright red blood per rectum
based on age :
<40 and obvious source no additional evaluation
40-50 sigmoidoscopy
>50 colonsocopy

Pruritus ani : chronic itch/scratch
Should be biopsied & complete assessment :
Persist pruritic lesion after adequate treatment
Anal pain with fever and inability to void signals
perineal sepsis
Warts or suspicious of verrucous carcinoma
Epidemiology
Second most common solid cancer globally
Risk related to Age and family history
Genetic risk
FAP
HNPCC (hereditary non polyposis colorectal cancer =
Lynch Syndrome)
Juvenile Polyposis
Environmental factors
Alcohol, obesity, Diabetes

Symptoms : Often none, altered bowel habit, Hematochezia,
LOW, Malaise, Iron deficiency anaemia
Investigation : Colonoscopy, Barium Enema/CT colography
Management : Resection, chemotherapy, radiation
TERIMA KASIH

KULIAH GASTRO OKTOBER
2011
Definition: Reflux of gastric contents (acid) into
oesophagus
Symptoms:
May be asymptomatic;
Heartburn, retrosternal chest pain
Regurgitation of gastric contents
Acidbrash, waterbrash (watery sensation in mouth)
Atypical chest pain
Nocturnal cough (exacerbation of asthma)
Dysphagia (long term symptoms)
Mechanism : GO junction incompetence
Due to transient LOS relaxation (tLOSR) (Common GERD)
Hypotensive LOS (More severe GERD)
Anatomical disturbance of LOS (Hiatus Herni)
Exacerbated by: Obesity, caffeine, alcohol, smoking,
fatty meal, medication, pregnancy
(hormonal/anatomic)
Drugs known to lower LOS pressure: calcium channel
blockers, beta-agonists, anti-cholinergic
medications, alphablockers, theophylline,
progesterone, morphine, dopamine and nitrates
Diagnosis : Endoscopy (gold standard), barium meal (may be helpful
for hiatus hernia), manometry/pH studies, PPI test
Complications
Esophageal : esophagitis, bleeding, stricture, Barretts esophagus,
adenocarcinoma
Extra-esophageal : laryngitis, carcinoma , Tracheal stenosis, Asthma,
Aspiration pneumonitis, Chronic cough, Dental erosion
Management
Lifestyle
Medication :
Proton pump Inhibitor (omeprazole, pantoprazole, rabeprazole,
esomeprazole, lanzoprasole)
H2Blocker (ranitidin, cimetidin, famotidin)
GI motility regulator ( primperan, domperidome, cisapride)
Surgery- Hiatus hernia repair
Investigation
Unnecessary : if typical syndrome in young (<50
probably normal
If alarm symptoms present (GI bleeding, anemia, age >50,
abnormal laboratory tests) Need to exclude:
In young: Coeliac disease and IBD
In edlerly: Colorectal cancer, Coeliac disease, IBD
Management
Supportive, Reassurance and explanation
Symptomatic : Analgaesia (antispasmodic)
Dietary
Psychological : Counselling, Antidepressants
Dyspepsia : chronic or recurrent discomfort centered
in the upper abdomen
The cause : functional/non-ulcer dyspepsia (specific
etiology is not identified most common), peptic
ulcers and gastroesophageal reflux, gastric and
pancreatic cancers
Management:
Endoscopy
Trial of empiric antisecretory (PPI) drug therapy, prokinetics
drugs
Testing for H. pylori infection followed by Tx if positive
Mechanism
Hp infection causing gastrin release and local
inflammation
Loss of mucosal defence (protective factor):
decrease mucous+bicarbonate, prostaglandins,
blood flow (NSAID)
Diagnosis
Non-invasive diagnosis of Hp
Endoscopy
Barium Meal


Complications
Haemorrhage
Perforation/penetration
Gastric outlet obstruction
Management
Complications : GI bleed, perforation
Healing the ulcer
Eradicate Hp
Treat with PPI
Prevent recurrence
Ensure eradication Hp
Longterm PPI prophylaxis if need NSAID (COX-2 selective)