Pleno 2

Kelompok 6
Kelompok 6
• Tutor : dr. Kumala & dr. Samuel
• Ketua : Haraka (405150178)
• Sekretaris :Gregorius Steven ( 405150113)
• Penulis : Kristo Hadi Audric (405150059)
• Anggota :
– Randy W (405150014)
– Anastasya Claudya (405150025)
– Anggela Oktaviani (405150039)
– Velisa J (405150073)
– Novia A (405150103)
– Michele W (405150167)
– Irwan S (405150170)
– Wulandari K (405150184)
 Problem 2
• A 55-year-old woman presented to her family physician
complaining of a month history of stomachahe which is occasionally
accompanied by nausea and bloating. The pain, which sometimes
awakened her at night,initially occurredseveral times a day between
meals. She drinks 3-5 cups black coffee throughout the day. She
often takes diclofenac tablet for her knee pain.

• She denied any changes in stool consistency or color

• Abdominal examinataions showed an epigastric tenderness on

palpation of the upper abdomen. All other labolatory values were
within normal limits

• What can you learn from the problem?

 Learning issues
• Learning issues :
1. Describe the anatomy,histology,and physiology
od the upper gastrointestinal tract
(gastric,duodenum)
2. Describe biochemical process in gaster, bile and
pancreas
3. Describe gastritis
4. Describe Dispesia
5. Describe GERD
6. Describe Gastric/duodenal Ulcer
LI1 : Describe the anatomy,histology,and
physiology od the upper gastrointestinal
tract (gastric,duodenum)
ANATOMY
 Figure 2.30. Abdominal part of esophagus and stomach.
A. The stomach and the greater and lesser omenta are shown. The left part
of the liver is cut away so that the lesser omentum and the omental foramen
(entrance to omental bursa) can be seen. The extent of the intact liver is
indicated by a dotted line. The stomach is inflated with air.
 Figure 2.30. Abdominal part of esophagus and stomach.
B. The internal surface (mucous membrane) is demonstrated. The longitudinal gastric folds, or
rugae, disappear on distension. Along the lesser curvature, several longitudinal mucosal folds
extend from the esophagus to the pylorus, making up the gastric canal along which ingested
liquids pass. C. The pylorus is the significantly constricted terminal part of the stomach. The pyloric
orifice is the distal opening of the pyloric canal into the duodenum.
The muscle layers of the oesophageal
and gastric walls
 Figure 2.31. Omental bursa and stomach bed.
A. In this anterior approach to the omental bursa, the greater omentum and gastrosplenic
ligament have been cut along the greater curvature of the stomach, and the stomach has been
reflected superiorly to open the bursa anteriorly. At the right end of the bursa, two of the
boundaries of the omental foramen can be seen: the inferior root of the hepatoduodenal ligament
(containing the portal triad) and the caudate lobe of the liver.
 Figure 2.31. Omental bursa and stomach bed.
B. The stomach and most of the lesser omentum have been excised, and the peritoneum of the
posterior wall of the omental bursa covering the stomach bed is largely removed to reveal the
organs in the bed. Although adhesions, such as those binding the spleen to the diaphragm here,
are common postmortem findings, they are not normal anatomy.
Posterior relations of the stomach.
Arterial Supply to Stomach
 Rami Esophageales
A. Gastrica
sinistra
Cabang ke lambung
Arteriae gastrica
breves
Cabang-cabang ke
A. Splenica dalam lien
Truncus
Celiacus Arteria Gastro-
omentalis sinistra
A.
Pancreaticoduodenalis
A. Gasroduodenalis superior
A. Gastro-omentalis
dextra
A. Hepatica
communis Arteria gastrica dextra

A. Hepatica propria A. Hepatica sinistra

A. Hepatica dextra
Veins of stomach, duodenum, and spleen
Lymphatic drainage of stomach
Innervation of stomach and small intestine

Distribution of the vagal nerves to the stomach. The two

commonest variations in the anterior vagus are shown in pink.
A, Multiple main trunks. B, Low origin of the hepatic/pyloric
branch lying close to the lesser curvature.
• The duodenum is divisible into
four parts:
a. Superior (first) part: short
(approximately 5 cm) and lies
anterolateral to the body of the
L1 vertebra.
b. Descending (second) part: longer
(7-10 cm) and descends along
the right sides of the L1-L3
vertebrae.
c. Horizontal (third) part: 6-8 cm
long and crosses the L3 vertebra.
d. Ascending (fourth) part: short (5
cm) and begins at the left of the
L3 vertebra and rises superiorly
as far as the superior border of
the L2 vertebra.
Artery of duodenum
Veins of stomach, duodenum, and spleen
Lymphatic drainage of stomach
histology
Esophago-gastric
junction

Eroschenko VP. Atlas histologi diFiore ed 11. 2012

• In the fundus and body the gastric glands themselves
fill most of the mucosa, with several such glands
formed by branching at the isthmus or neck of each
gastric pit.
• There are 4 important properties of each as follow :
1. Mucous neck cells
2. Parietal cells
3. Chief(zymogenic) cells
4. Enteroendocrine cells
There are cardia and pylorus glands  lack of parietal
and chief cell
Pyloric region

http://www.histology.leeds.ac.uk
Small intestine
 Review

Wheater’s functional histology

p.274
physiology
 Stomach
• 3 main functions
– Store ingested food until it can be emptied into
the small intestine
– Secretes HCl & enzymes, begin protein digestion
– Stomach’s mixing movement  ingested food
pulverized & mixed with gastric secretions  thick
liquid mixture (chyme)

– Gastric’s motility
• Filling, storage, mixing, emptying
 Gastric filling
• Volume about 50 ml; can expand to 1l during
a meal
• Folds of gastric get smaller & nearly flatten
out as stomach relaxes slightly (receptive
relaxation)  enhance stomach to
accomodate the extra volume of food with
little rise in stomach pressure
– Triggered by the act of eating & mediated by the
vagus nerve
 Gastric storage (body of stomach)
• Interstitial cells of Cajal  generates slow
wave potential (Basic electrical rhythm) 
occurs continuously with or without muscle
contraction  food is stored in the relatively
quite body without being mixed

• Fundus contains only pocket of gas

Gastric mixing (antrum of stomach)
• Strong antral peristaltic  mix food & gastric
juice ( chyme)  propels the chyme
towards pyloric sphincter
• Tonic contraction of pyloric sphincter keeps it
almost closed  bulk of the antral chyme
tumbled back into the antrum  propeled
forward  tumbled back again as the new
peristaltic wave advances
 Gastric emptying
• Gastric factor
– Amount of chyme; stomach distention  strecth
of smooth muscle, intrinsic plexuses, vagus nerve,
gastrin  gastric motility >>
– Degree of fluidity
• Duodenum factor
– Fat, acid, hypertonicity, & distention
Mechanism of H & Cl ions secretion
• Function of HCl:
– Activate pepsiongen 
pepsin
– Aids breakdown of
connective tissue &
muscle fibers, reducing
food into smaller
particles
– Denaturates protein
– Along with lysozyme 
kills microorganism
Pepsinogen, activated  protein digestion

Pepsin’s autocatalytic activity

 Mucus
• Lubricating properties, protects gastric
mucosa
• Protect the stomach wall from self-digestion
because of pepsin
– doesn’t affect pepsin activity in the lumen
• Being alkaline  neutralizing HCl
– Doesn’t interfere with the function of HCl in the
lumen
 Regulatory pathways  parietal & chief cells

• Acetylcholine  short local reflexes & vagal

stimulation  parietal & chief cells, G & ECL cells
• G cells  secrete gastrin
– Main factor for increased HCl secretion by stimulating
ECL cells to release histamine
• Enterochromaffin like cells  paracrine histamine
– Speed up HCl secretion, potentiates ACh & gastrin
• D cells  paracrine somatostatin
– Negative feedback fashion
LI 2 : Describe biochemical process
in gaster, bile and pancreas
 Major Action
Hormone Site of Synthesis
Stimulates Inhibits
Gastrin G cells in stomach Gastric acid secretion
Ghrelin Gr cells in GH secretion Lipid metabolism
stomach Appetite and Fat utilization in
perception of hunger adipose tissue
Cholecystoki I cells in Gallbladder Gastric emptying
nin duodenum and contraction;
jejunum Pancreatic enzyme
and bicarbonate ion
secretion; pancreatic
growth
Secretin S cells in Pancreatic enzyme, Gastric acid
duodenum bicarbonate ion secretion
secretion; pancreatic
growth
Gastric K cells in Insulin release Gastric acid
inhibitory duodenum and secretion
peptide jejunum
(GIP)
Ross MH, Pawlina W. Histology A Text and Atlas with Correlated Cell and Molecular
 Major Action
Hormone Site of Synthesis
Stimulates Inhibits
Candidate Hormones
Pancreatic PP cells in Gastric emptying Pancreatic
polypeptide pancreas and gut motility enzyme and
bicarbonate
secretion
Peptide YY L cells in ileum Electrolytes and Gastric acid
and colon water absorption in secretion; Gastric
the colon emptying; Food
intake
Glucagon- L cells in ileum Insulin release Gastric acid
like and colon secretion; Gastric
peptide-1 emptying
(GLP1)
Paracrine Hormones
Somatostati D cells in mucosa Gastrin release;
n throughout GI Gastric acid
tract secretion;
Ross MH, Pawlina W. Histology A Text and Atlas with Correlated Cell and Molecular
Release of other
 Major Action
Hormone Site of Synthesis
Stimulates Inhibits
Neurocrine Hormones
Bombesin Stomach Gastrin release
Enkephalins Mucosa and Smooth muscle Intestinal
smooth muscle contraction secretion
throughout GI
tract
Vasoactive Mucosa and Pancreatic enzyme Smooth muscle
inhibitory smooth muscle secretion; Intestinal contraction;
peptide throughout GI secretion sphincter
(VIP) tract contraction

Ross MH, Pawlina W. Histology A Text and Atlas with Correlated Cell and Molecular
LI 3 : Describe gastritis
 Gastritis

Definition • Gastritis : inflammation of gastric mucosa

• Gastropathy : cell damage followed by regeneration with
minimal inflammation
Classificat • Acute: Erosive, Non-erosive
ion • Chronic: Non atrophic chronic gastritis, Atrophic gastritis:,
Autoimmune gastritis, Multifocal atrophic gastritis
• Special forms of gastritis: Reactive gastropathy (chemical
gastropathy), Radiation, Lymphocytic, Non-infectious
granulomatous gastritis, Eosinophilic gastritis, Collagenous
gastritis, Infectious gastritis
Robbin’s basic pathology. 9th ed.
 Acute Gastritis
• Etiology: Candidiasis,
– Drugs → NSAIDs; histoplasmosis,
cocaine; iron; phycomycosis
chemotherapeutic – Parasitic infection →
agents anisakidosis
– Potent alcoholic – Acute stress (shock)
beverages → whisky, – Radiation
vodka, and gin
– Allergy and food
– Bacterial infections → poisoning
H pylori (most
– Bile: The reflux of bile
frequent), H heilmanii,
from the small
Pathoph • Erosive gastritis: because of exposure to NSAIDs, alcohol,
ysiology stress, bile reflux
• Exposure → reduction of prostaglandin (for protection of
mucosa from gastric acid) or reduce bicarbonate secretion
→ injury of mucosa
• Non erosive gastritis: generally caesed by H. pylori
• Infection H. Pylori → producing toxin and enzymes → induce
IL 8 → attracts PMN and monocytes → inflammation (acute
gastritis)
Sign and • Gnawing or burning epigastric distress
Sympto • Upper abdominal discomfort
ms • Nausea and/or vomitting
• Loss of appetite
Diagnosi • Complete blood count: to assess for anemia because of
s gastrointestinal bleeding
• Stool test: check for blood in the stool as the sign of
stomach bleeding
• Urea breath test: The patient swallows a capsule, liquid, or
 Endoscopy

Acute gastritis with superficial erosion

http://emedicine.medscape.com/article/175909-overview
 Radiologic findings
Four signs of acute gastritis:
• Thick folds: greater than 5 mm in caliber
found in patient who is symptomatic → H.
Pylori infection
• Nodules of gastric mucosa: small in size,
usually seen in distal
• Coarse area gastrica: 1-3mm enlargement
• Gastric erosion
Erosive gastritis
http://www.medscape.com/viewarticle/410726_2

Thick fold
https://www.mypacs.net/cases/CHRONIC-GASTRITIS-10093144.html
 Histologic findings

https://www.jhmicall.org/GDL_Disease.aspx?CurrentUD
V=31&GDL_Cat_ID=551CDCA7-A3C1-49E5-B6A0-
C19DE1F94871&GDL_Disease_ID=80AD1118-6659-
4B04-B560-71B95E3B7FA9
 Medication
• Antacids: containing aluminum and
magnesium can help relieve symptoms of
gastritis by neutralizing gastric acids
• H2 receptor inhibitor: competitive inhibition
of histamine at the histamine 2 (H2) receptor
• Proton pump inhibitor: inhibitors of the
proton (acid) pump (ie, the enzyme H+,K+-
ATPase)
 H2 receptor inhibitor
Drugs Usual Dose for Usual Dose for Usual Dose for
Acute Gastroesopha Prevention
Duodenal or geal of Stress–
Gastric Ulcer Reflux Disease Related
Bleeding
Cimetidine 800 mg HS or 800 mg bid 50 mg/h
400 mg bid continuous
infusion
Ranitidine 300 mg HS or 150 mg bid 6.25 mg/h
150 mg bid continuous
infusion or 50
mg IV every
6–8 h
Nizatidine 300 mg HS or 150 mg bid -
150 mg bid
Famotidine 40 mg HS or 20 mg bid 20 mg IV every
20 mg bid 12 h
HS: bedtime
 PPI
Drugs Usual dosage for peptiic ulcer
or GERD
Omeprazole 20–40 mg qd
Esomeprazole 20–40 mg qd
Lansoprazole 30 mg qd
Dexlansoprazole 30–60mg qd
Pantoprazole 40 mg qd
Rabeprazole 20 mg qd
 Complication
• Bleeding from an erosion or ulcer
• Limiting the adequate transfer of food from
the stomach to the small intestine
• Dehydration from vomiting
• Renal insufficiency as a result of dehydration
 Chronic Gastritis
Epidemiolo • Autoimmune gastritis is a relatively rare disease, most
gy frequently observed in individuals of northern European and
black people
• Patient w/ autoimmune gastritis usually present w/ pernicious
anemia
• H pylori gastritis is usually acquired during childhood, and
complications typically develop later
• H. pylori infection related to socio-economic factors
Etiology • Non atrophic chronic gastritis: H. pylori
• Atrophic gastritis: Autoimmune gastritis: autoimmunity, H.
pylori, Multifocal atrophic gastritis: H. pylori
• Special forms of gastritis: Reactive gastropathy (chemical
gastropathy): NSAID, bile reflux, Radiation: radiation injury,
Lymphocytic: unknown, Non-infectious granulomatous gastritis:
• H. pylori associated
chronic gastritis:
Infection H. pylori
→ producing toxin
and enzymes →
induce IL 8 →
attracts PMN and
monocytes →
inflammation
(acute gastritis) →
neutrophils
synthesize
Leukotriene B4 →
cytotoxic to gastric Yamada’s Textbook of Gastroenterology. 6th ed.

epithelium →
functional changes
in stomach
• Atrophic gastritis:
– Autoimmune:
• Patient whose already
has autoimmune
disease: Anti-parietal &
anti-IF antibodies →
diffuse atrophy of
parietal and chief cell →
IF deficiency →
cobalamine deficiency →
pernicious anemia
• Infection H. pylori → http://emedicine.medscape.com/article/176036-
mimicry → autoimmune overview#a5

– Multifocal atrophic
gastritis
 SS
• Gnawing or burning epigastric distress
• Upper abdominal discomfort
• Nausea and/or vomitting
• Loss of appetite
• Autoimmune gastritis: patient is pale and has
slightly icteric skin and eye
 Laboratory studies
• Complete blood count
• Stool test
• Urea breath test
• Antiparietal and anti–intrinsic factor (IF)
antibodies in the serum
• Low serum cobalamin (vitamin B-12) levels
(<100 pg/mL)
• Biopsy
 Medication
• Antibiotics:
– Amoxicillin 1 g PO q12hr for 14 days with lansoprazole
(30 mg) and clarithromycin (500 mg) or 1 g PO q8hr
for 14 days with lansoprazole (30 mg) (in patients
intolerant of, or resistant to, clarithromycin)
• Proton pump inhibitor:
– Omeprazole: 20 mg PO q12hr for 10 days, w/
Amoxicillin 1000 mg PO q12hr, and Clarithromycin 500
mg PO q12hr for 10-14 days
– Lansoprazole: 30 mg + amoxicillin 1 g + clarithromycin
500 mg PO q12hr for 10-14 days
• Bismuth
LI 4 :Describe Dispesia
Dyspepsia
 Functional Dyspepsia
• Dyspepsia refers to symptoms originating in the upper GI tract; is
used to describe upper abdominal pain or discomfort often
exacerbated with eating, early satiety, postprandial abdominal
bloating or distention, and nausea
• Rome III criteria for functional dyspepsia including the following
requirements (these features be fulfilled for the previous 3 months
with symptom onset at least 6 months before diagnosis):
– The presence of one or more of the following:
bothersome postprandial fullness, early satiation,
epigastric pain, epigastric burning.
– No evidence of structural disease (including at upper
endoscopy) that is likely to explain the symptoms.
• Etiology
• Delayed gastric emptying and antral
hypomotility: antral hypomotility or small
intestine dysmotility → delayed gastric
emptying
• Regional gastric dysfunction (impaired fundic
accommodation and antral distention): poor
receptive relaxation or accommodation of the
proximal stomach → rapid transit from the
proximal stomach to antrum
• Gastric myoelectric abnormalities: measured
by ECG to measure bradygastria or tachygastria
• Visceral hypersensitivity
Pathophisiology
• Motility
– The abnormalities range from delayed to
accelerated gastric emptying, abnormal antral and
fundic contractions, and accommodation issues in
the fundus and antrum
– Delayed gastric emptying of solids was associated
with postprandial fullness and vomiting
• Acid exposure
– Might be hypersensitivity to normal acid secretion
• Food intolerance
– Suggests a hypersensitivity
• Central nervous system-stimulus processing
– Related with familial aggregation, sleep
dysfunction, somatization, and anxiety.
– Common triggers which may initiate pathologic
cycle processes involving gastrointestinal system
Diagnostic Criteria ROME III
• Treatment
• Promotility agent:
– Domperidone is a peripherally acting dopamine
antagonist that is known to promote gastric
emptying and antropyloric motility
– Cisapride stimulates gastrointestinal motility
through its action as a partial 5HT4 agonist
• Antidepressant
• Cognitive psychotherapy
LI 5 : Describe GERD
 GERD
GERD
 is an esophageal mucosal injury that occurs secondary to
retrograde movement of gastric  content into the esophagus.

http://www.hopkinsmedicine.org
 ETIOLOGY
– Poor/abnormal LES function
• short LES (the shorter the LES the lower the tonus)
• Hormonal factors (during pregnancy increase in progesterone causes
decreased LES tonus)
– hiatal hernia
– Consumption of drugs(antikolinergik, beta adrenergik, theofilin, opiat, etc)
– Poor esophageal clearance
• common in elderly population or in patients with achalasia, stroke, or
collagen vascular disease such as scleroderma.
– Delayed gastric emptying
• due to anatomic obstruction of the gastric outlet as seen in pyloric
stenosis
 EPIDEMIOLOGY

GERD occurs in all age groups. The prevalence of GERD increases

in people older than 40 years.
 PATHOPHYSIOLOGY
• The esophagus,LES, and stomach
can be envioned as a simple
plumbing circuit who work
together.
• The abnormalities that
contribute to GERD can stem
from any component of the
system.
1. Poor esophageal motility
decreases clearance of acidic
material.
2. A dysfunctional LES allows reflux
of large amounts of gastric juice.
3. Delayed gastric emptying can http://www.medscape.org
increase the volume and pressure
leading to GERD.
 SIGN & SYMPTOM

• The most typical symptoms of

GERD(Intra esofageal)
Heartburn
Regurgitation
Disphagia

• Abnormal reflux can cause

atypical (extraesophageal)
Coughing and/or wheezing
Hoarseness, sore throat
Otitis media
Noncardiac chest pain
Enamel erosion or other dental
manifestations
http://www.medscape.org
 DIAGNOSIS

1. Upper gastrointestinal endoscopy

• Upper endoscopy is the first diagnostic test in the evaluati
on  of  GERD
• Evaluate Microscopic changes of the esophageal mucosa
and Eliminating other pathological conditions that can
cause gerd
• If not found Mucosa Break  NERD (Non Erosive Reflux
disease)
2. Barium Esophagram

http://www.hopkinsmedicine.org
3. Esophageal Manometry

involves the placement of a

pressure sensitive catheter
into the esophagus .The test
permits evaluation of the
strength and coordination of
muscle contractions, as well
as the strength and relaxation
function of the LES. http://www.hopkinsmedicine.org
4. PH Monitoring
also called 24-hour pH studies. It provides
information on the severity and pattern of
reflux. The information is helpful both to
confirm the impression of reflux and to
tailor
therapy for the individual patient .

Ph below 4 at a distance of 5 cm above LES

 GERD

http://www.hopkinsmedicine.org
5. Gerd Q

an instrument of questionnaire
developed to assist
establishing the diagnosis of
GERD and measuring response
to therapy.

http://www.actamedindones.org/index.php/ijim/article/viewFile/98/94
6. PPI test.
Is an empirical therapy to assess GERD symptoms by
providing high-dose PPI for 1- 2 weeks pending the respons.
Done when there is no endoscopic modality,Ph metry etc.
 Avoid large meals.

GERD Avoid acidic foods (citrus- and tomato-

based products), alcohol, caffeinated
beverages, chocolate, onions, garlic, and
peppermint.
Therapeutic Decrease dietary fat intake.

Management Avoid lying down within three to four hours

after a meal.

Avoid medications that may potentiate

GERD symptoms, including calcium
• Lifestyle channel blockers, beta agonists, alpha-
adrenergic agonists, theophylline, nitrates,
modifications and some sedatives.
Elevate the head of the bed 10 to 20 cm (4
to 8 inches).

Avoid wearing clothing that is tight around

the waist.
Lose weight.
Stop smoking.
 GERD Therapetic Management
DRUGS
Drug Farmakokinetik
Antacid  neutralize acid or acidic food without affecting subsequent acid secretion.
Control mild to moderate symptoms. Given2 hours after meals and every will
sleep.
Dosage: 4 x 1 tablespoon.
Antagonis Receptor H2  block  histamine-stimulated  acid  secretion.inhibit interaction of histamine at
(Ranitidine,Cimetidine,Famotidin the H 2 receptors  work directly to inhibit acid scretion.
e) Raitidine :4 x 150 mg
Simetidine :2x 800 mg or 4x 400mg
Faamotidine : 2 x 20mg
Nizatidine : 2x 150 mg
Prokinetik drugs that enhance motor activity of the smooth muscle (characteristic of GI
(Metoclopramide) tract). Increase the pressure of les and lower the reflux of gastric contents. This
drug serves to accelerate the gastric empty
Metoclopramide : 3 x10 mg
Domperidone : 3 x 10-20mg
Cisapride : 3 x10 mg
PPI (Proton Pump Inhibitor) DOC Are drugs that block the final common pathway of acid secretion. PPIs block
(Omeprazole) the effects of all three major pathways
(histamine, acetylcholine, and gastrin) for acid stimulation.
Omeprazole: 2 x 20 mg
Lansoprazole : 2x 30mg
Pantoprazole : 2 x40 mg
Rabe prazole :2x10 mg
Esomeprazole :2x40 mg
LI 6 : Describe Gastric/duodenal
Ulcer
 Gastric Ulcer
Definition • Ulcers are defined as breaks in the mucosal surface >5 mm in size, with
depth to the submucosa.
• Gastric ulcers are defect in the gastric or mucosa that extend through the
muscularis mucosa.
Risk Factor • Helicobacter pylori and NSAIDs
• Chronic obstructive lung disease
• Chronic renal insufficiency
• Current tobacco use
• Older age
• Coronary heart disease
• Former alcohol
• African-American race
• Obesity
• Diabetes
Pathophysiology • Gastric ulcers typically are associated with widespread gastritis
• Acid-peptic inflammation is believed to occur when there is an imbalance
between cytotoxic and cytoprotective factors in the upper gastrointestinal
tract.
Classification • Type I : occur in the gastric body and tend to be associated with low gastric
acid production
• Type II : occur in the antrum and gastric acid can vary from low to normal
• Type III : occur within 3 cm of the pylorus and are commonly accompanied
by DUs and normal or high gastric acid production
• Type IV : are found in the cardia and are associated with low gastric acid
production.
Sign and • Epigastric pain described as a burning or gnawing discomfort, an ill-
Symptoms defined, aching sensation or as hunger pain
• Discomfort may actually be precipitated by food
• Nausea
• Weight loss
Diagnosis • Biopsy
• Upper GI tract endoscopy
• Radiographic
Treatment •• Serologic
Protectivetesting
foods that contain phenolic antioxidants such as cranberries or
• The fecal
ginger H. pylori
extracts (Hp) antigen
(Zingiber test which may have the capacity to help
officinale),
eradicate H. pylori
Complication • Gastrointestinal bleeding : occur more often in individuals >60 years of age
• Perforation
• Gastric outlet obstruction : the least common ulcer-related complication,
occurring in 1–2% of patients
 Duodenal Ulcer
Definition • An ulcer is defined as disruption of the mucosal integrity of the
stomach and/or duodenum leading to a local defect or excavation
due to active inflammation.
• Ulcers are defined as breaks in the mucosal surface >5 mm in size,
with depth to the submucosa.
Pathophysiolo • DUs occur most often in the first portion of the duodenum (>95%),
gy with ∼90% located within 3 cm of the pylorus. They are usually ≤1
cm in diameter but can occasionally reach 3–6 cm (giant ulcer).
Ulcers are sharply demarcated, with depth at times reaching the
muscularis propria. The base of the ulcer often consists of a zone of
eosinophilic necrosis with surrounding fibrosis. Malignant DUs are
extremely rare.
Epidemiology • Age : Peak age: 30-40 years, second peak in old age
• Sex : Male predominance
• Higher in Asia
 Causes
• H. pylori
• NSAIDs including aspirin
 Pathophysiology

Longo DL, Fauci AS. Harrison’s

Gastroenterology and Hepatology.
2nd ed. New York: McGraw-Hill,2013.
Longo DL, Fauci AS. Harrison’s
Gastroenterology and Hepatology.
2nd ed. New York: McGraw-Hill,2013.
Sign and • Epigastric tenderness
Symptoms • Gnawing or burning sensation and occurs 2-3 hours after
meals
• epigastric pain or discomfort that occurs in the fasted
state, typically at night or 2 to 3 hours after meals, with
food relief.
• Syrchadian ryhtm 11-2am
• Pain is typically reported as burning, aching, gnawing, or
as a “hunger pain” or discomfort.
Diagnosis • Physical examination
• Epigastric tenderness : pain may be found to the right of
the midline in 20 % patients
• Important for discovering evidence of ulcer complication
• Radiographic (barium study)
• Endoscopic
Longo DL, Fauci AS. Harrison’s Gastroenterology and
Hepatology. 2nd ed. New York: McGraw-Hill,2013.
 Longo DL, Fauci AS. Harrison’s
Gastroenterology and Hepatology. 2nd
ed. New York: McGraw-Hill,2013.

Yamada, T. 2003.
Textbook of
Gastroenterology. 4th
edition. Volume 1.
Philadelphia : Lippincott
• Surgery
– Vagotomy
– Pyloroplasty
– Gasjejunostomy
– rarely partial gastrectomy
DD • NUD
• Proximal GI tumors
• Gastroesophageal reflux
• Vascular disease
• Pancreaticobiliary disease (biliary colic, chronic
pancreatitis)
• Gastroduodenal Crohn’s disease
Complicat • GI Bleeding
ion • Perforation
• Gastric outlet obstruction
 Duodenal Ulcers in Pediatric
• H.pylori is responsible for more than half of ulcers in
the stomach and duodenum in adults, but lesser role in
childhood ulcer disease.
• Risk factor: low socioeconomic status, poor sanitation
• Highest incidence : developing country
• Clinical manifestations : occurs several hours after
meals and often awakens patients at night. Eating
tends to relieve the pain
• Diagnosis: endoscopy
• Treatment: H2 receptor antagonist , Proton pump
inhibitor (4-8 weeks)
 NSAID Related Ulcer
Epidemiolog • NSAIDs represent a group of the most commonly used medications.
y • Side effects and complications due to NSAIDs are considered the most common
drug-related toxicities.
• The spectrum of NSAID-induced morbidity ranges from nausea and dyspepsia
(prevalence reported as high as 50–60%) to a serious GI complication such as
endoscopy-documented peptic ulceration (15–30% of individuals taking NSAIDs
regularly) complicated by bleeding or perforation in as many as 1.5% of users
per year.
Risk Factor • Possible risk factors include concomitant infection with H. pylori, cigarette
smoking, and alcohol consumption.
Pathophysio • Prostaglandins play a critical role in maintaining gastroduodenal mucosal
logy integrity and repair.
• Animal studies have demonstrated that neutrophil adherence to the gastric
microcirculation plays an essential role in the initiation of NSAID-induced
mucosal injury.
• Injury to the mucosa also occurs as a result of the topical encounter with
NSAIDs.
• Aspirin and many NSAIDs are weak acids that remain in a nonionized lipophilic
Harrison Internal Medicine Gastroenterology and Hepatology
PG-Dependent Mechanism in Stomach
Injury
• Since PGs play a critical role in maintaining gastric
mucosal defense system, the inhibition of COX leading
to decreased mucosal PGs is considered as the most
important in the pathogenesis of NSAID-induced
gastric damage.
• COX-1 is constitutively expressed in most of tissues
including stomach and responsible for maintaining
gastric mucosal integrity at base line, whereas COX-2
participates in inflammation.
• Gastric injury was thus considered to be ascribed to
gastric mucosal PG deficiency by COX-1 inhibition.
The ‘trapping’ theory
• Most NSAIDs are weak organic acids. In gastric juice, they are non-ionized
and lipid soluble. These NSAIDs diffuse across gastric mucosal epithelial cell
membranes into the cytoplasm, where pH is neutral. In neutral pH, NSAIDs
are converted into the re-ionized and relatively lipophobic form. Therefore
NSAIDs are trapped and accumulate within cells, leading to the cellular
injury.
Mitochondria, lipid peroxidation, and apoptosis
• Mitochondrial respiratory chain is the major source of reactive oxygen
species (ROS), which are mainly generated at Complex I and III of the
respiratory chain. More importantly, the mitochondrial respiratory chain is,
at the same time, an important target for the damaging effects of ROS. ROS
from mitochondria play an important role in the release of cytochrome c
and other pro-apoptotic proteins, which can trigger caspase activation and
apoptosis.
• Mitochondria are considered as the target intracellular organelle of
absorbed NSAIDs. NSAIDs inhibit, or uncouple, oxidative phosphorylation to
dissipate the mitochondrial transmembrane potential (MTP), leading to the
liberation of cytochrome c from mitochondrial intermembranous space into
cytosol and to the release of ROS such as superoxide (O2•−) and hydrogen
peroxide (H2O2), thereby causing caspase 9 and caspase 3 activation and
cellular lipid peroxidation, all resulting in cellular apoptosis
Pathophysiology of NSAID-Induced
Small Intestinal Injuries
Clinical features of complicated peptic
ulcer disease
• Acute complicated PUD: upper GI bleeding
(hemorrhage), severe pain (perforation or
penetration), and vomiting (gastric outlet
obstruction)
• Chronic complications: iron-deficiency anemia
and chronic gastric outlet obstruction
secondary to scarring
 Therapies
 Discontinuation of the drug if possible in conjunction with a
PPI to promote healing
 Concurrrent H. pylori infection should also be sought.
 PPIs accelerate ulcer healing in this setting and are
preferred to H2RAs. Misoprostol and sucralfate are inferior
to PPI, particularly if NSAIDs are continued, and the utility
of misoprostol is limited by its GI side effects.
 Management should then be directed at assessment and
modification of risk factors, with secondary preventative
strategies.
 Maintenance therapy with a PPI is particularly important
for patients who continue or resume NSAID treatment.
Prevention
 H. Pylori Related Ulcer

Etiology • Helicobacter pylori colonizes the stomachs of 50% of the

world’s human population throughout their lifetimes.
• Colonization with this organism is the main risk factor for
peptic ulceration.
• H. pylori is a gram-negative bacillus that has naturally
colonized humans.
• It lives in gastric mucus, with a small proportion of the
bacteria adherent to the mucosa and possibly a very small
number of the organisms entering cells or penetrating the
mucosa; its distribution is never systemic.
• The organism has several acid-resistance mechanisms,
most notably a highly expressed urease that catalyzes urea
hydrolysis to produce buffering ammonia.
Etiology • H. pylori is microaerophilic (requiring low levels of
oxygen), is slow-growing, and requires complex growth
media in vitro.
• In immunocompromised hosts, several nongastric
(intestinal) Helicobacter species can cause disease with
clinical features.
Epidemiol • The prevalence of H. pylori is >80% in most developing
ogy countries.
Risk • Crowding and maternal colonization.
Factor • Humans are the only important reservoir of H. pylori .
• Children may acquire the organism from their parents
(more often from the mother) or from other children.
• Pathophysiology
– H. pylori colonization induces a tissue response in the
stomach, chronic superficial gastritis, which includes
infiltration of the mucosa by both mononuclear and
polymorphonuclear cells.
– Colonization is accompanied by a considerable
persistent immune response, but these responses are
ineffective in clearing the bacterium.
– Most H. pylori–colonized persons do not develop clinical
sign, its related to bacterial strain differences, host
susceptibility to disease, and environmental factors.
– CagA affects host cell signal transduction, inducing
proliferative, and inflammatory changes.
– The secretion system - translocates soluble components
of the peptidoglycan cell wall into the gastric epithelial
cell - recognized by bacterial receptor Nod1 - stimulates
a proinflammatory cytokine response - enhanced gastric
inflammation.
– Patients with peptic ulcer disease or gastric adenocarcinoma
are more likely colonized by cag-positive strains.
– Other bacterial factors that are associated with increased
disease risk include adhesins, such as BabA and SabA, and
incompletely characterized genes, such as dupA.
– The best-characterized host determinants of disease are
genetic polymorphisms leading to enhanced activation of the
innate immune response.
– For example, colonized people with polymorphisms in the
interleukin (IL) 1 gene that cause the production of large
quantities of this cytokine in response to H. pylori infection
are at increased risk of gastric adenocarcinoma.
– Environmental cofactors are important in pathogenesis.
Smoking increases the risks of ulcers and cancer in H. pylori–
positive individuals. Diets high in salt and preserved foods
increase cancer risk, whereas diets high in antioxidants and
vitamin C are protective.
– H. pylori–induced inflammation diminishes the
number of somatostatin-producing D cells.
– Somatostatin inhibits gastrin release, gastrin
levels are higher than in H. pylori–negative
persons, and these higher levels lead to
increased ed acid secretion in the gastric
corpus.
Sign and • Many patients have upper gastrointestinal symptoms but
Symptoms have normal results in upper gastrointestinal endoscopy
(so-called functional or nonulcer dyspepsia.
• An ache or burning pain in your abdomen
• Abdominal pain that's worse when your stomach is empty
• Nausea
• Loss of appetite
• Frequent burping
• Bloating
• Unintentional weight loss
Staging • The first step is chronic gastritis, which is followed by the
second step, atrophic gastritis. The third step is intestinal
metaplasia, which may evolve into dysplasia. The last step
in this process is gastric adenocarcinoma.
• This process is very slow (ie, decades) and may stop at any
step because gastric cancers probably require several
other factors to develop, not only an H pylori infection.
Harrison Internal Medicine Gastroenterology and Hepatology
• Diagnosis
– Tests for the presence of H. pylori can be
divided into two groups: invasive tests, and
noninvasive tests.

Harrison Internal Medicine Gastroenterology and Hepatology

– Endoscopy often is not performed in the initial management
of young dyspeptic patients without “alarm” symptoms but is
commonly used to exclude malignancy in older patients.
– The presence of H. pylori urease leads to a pH alteration and
therefore to a color change, which often occurs within
minutes but can require up to 24 h.
– Histologic examination of biopsy specimens for H. pylori also
is accurate, provided that a special stain (e.g., a modified
Giemsa or silver stain) permitting optimal visualization of the
organism is used.
– Microbiologic culture is most specific but may be insensitive
because of difficulty with H. pylori isolation.
– Noninvasive H. pylori most consistently accurate test is the
urea breath test.
– In this simple test, the patient drinks a solution of urea
labeled with the nonradioactive isotope 13C and then blows
into a tube. If H. pylori urease is present, the urea is
hydrolyzed and labeled carbon dioxide is detected in breath
samples.
 – The stool antigen test is more convenient and
potentially less expensive than the urea breath test
but has been slightly less accurate in some
comparative studies.
– The simplest tests for ascertaining H. pylori status
are serologic assays measuring specific IgG levels in
serum.
• Differential diagnosis
– Pediatric/Adult : Cholecystitis, Crohn Disease,
Esophagitis, Gallstones (Cholelithiasis),
Gastroesophageal Reflux, Pancreatitis and
Pancreatic Pseudocyst
– Peptic Ulcer Disease
– Ureteropelvic Junction Obstruction
 Helicobacter
pylori infection
revealed by
endoscopy
(nodular
gastropathy).

http://emedicine.medscape.com/article/929452-overview
https://www.slideshare.net/doctorrao/helicobacter-pylori-
Harrison Internal Medicine Gastroenterology and Hepatology
Harrison Internal Medicine Gastroenterology and Hepatology
• Non-Pharmacological Treatment
– Foods such as berry juice and some dairy products may
have modest bacteriostatic effect on H pylori.
– Two randomized, placebo-controlled trials evaluated the
effect of probiotic food as an adjuvant to the standard
triple therapy for eradication of H pylori infection in
children and showed conflicting results.
– In a recent prospective study in adults, addition of
vitamin C to an H pylori treatment regimen of
amoxicillin, metronidazole, and bismuth can significantly
increase H pylori eradication rate.
• Prognosis and Complication
• The outlook for eradicating H pylori infection with
multidrug therapy is good, with reported efficacy
rates as high as 95%.
• Unsuccessful therapy often results from the
patient's noncompliance with the medication
regimen or from antimicrobial resistance.
• Once cure is achieved, long-term reinfection rates
are low. Among children living in developing
countries or among families with infected
members, reinfection rates may be increased
– PUD - Perforation, GI bleeding • Prevention
– Iron-deficiency anemia – Policies that support the
– Malignancy improvement of living
conditions, particularly in
– Gastric mucosa-associated
developing countries
lymphoid tissue (MALT)
lymphoma – For all patients with chronic
GI tract symptoms,
– Adenocarcinoma of the
appropriate referral for
gastric body and antrum
definitive diagnosis and
– Gastric-outlet obstruction treatment, which may help
– Increased susceptibility to effect a cure and prevent
enteric infections such as exposure to family members
salmonellosis and giardiasis and close contacts
due to H pylori- induced – Vaccines against H pylori
hypochlorhydria infection
 Advice and conclusion
• Patient is recommended to proceed with
upper gastroimtestinal endoscopy and
radiologic examination
• Patient must stop to consume more than 1
cup of coffe
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Hill, 2013.
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