Pemicu 2

Dessy 405150011
Anatomy
 Gaster = Venticulus = Stomach
• Esophagus – Duodenum
• As shelters of food to be digested become
“chyme”
• Regulate the flow of digested food into the small
intestine
• Capacity: ± 1.5 liters, can be dilated un til 2-3
liters
• The stomach capacity of newborn baby: ± 30 cc
• The most common is J-shaped
 Surface Anatomy of the Stomach
• In the supine position, the stomach commonly
lies in the right and left upper quadrants, or
epigastric, umbilical, and left hypochondriac
and lumbar regions.
The surface markings of the stomach in the supine position include the:
• Cardial orifice: which usually lies posterior to the 6th left costal
cartilage, 2-4 cm from the median plane at the level of the T11
vertebra.
• Fundus: which usually lies posterior to the left 6th rib in the plane of
the MCL.
• Greater curvature: which passes inferiorly to the left as far as the
10th left cartilage before turning medially to reach the pyloric antrum.
• Lesser curvature: which passes from the right side of the cardia to
the pyloric antrum; the most inferior part of the curvature is marked
by the angular incisure, which lies just to the left of the midline.
• Pyloric part of the stomach in the supine position: which usually
lies at the level of the 9th costal cartilages at the level of L1 vertebra;
the pyloric orifice is approximately 1.25 cm left of the midline.
• Pylorus in the erect position: which usually lies on the right side; its
location varies from the L2 through L4 vertebra.
 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 stomach also has two curvatures:
– Lesser curvature: forms the shorter concave border of the
stomach; the angular incisure (notch) is the sharp indentation
approximately two thirds the distance along the lesser
curvature that indicates the junction of the body and the
pyloric part of the stomach.
– Greater curvature: forms the longer convex border of the
stomach.
• Intermittent emptying of the stomach occurs when intragastric
pressure overcomes the resistance of the pylorus. It is normally
tonically contracted so that the pyloric orifice is reduced, except
when emitting chyme. At irregular intervals, gastric peristalsis
passes the chyme through the pyloric canal and orifice into the
small intestine for further mixing, digestion, and absorption.
 Peritoneal Formations
• An omentum is a double-layered extension or fold of
peritoneum that passes from the stomach and proximal
part of the duodenum to adjacent organs in the abdominal
cavity.
– The greater omentum is a prominent peritoneal fold that hangs
down like an apron from the greater curvature of the stomach
and the proximal part of the duodenum (Fig. 2.19A, C, & E).
After descending, it folds back and attaches to the anterior
surface of the transverse colon and its mesentery.
– The lesser omentum connects the lesser curvature of the
stomach and the proximal part of the duodenum to the liver
(Fig. 2.19B & D); it also connects the stomach to a triad of
structures that run between the duodenum and liver in the free
edge of the lesser omentum (Fig. 2.17).
Figure 2.19. Principal formations of peritoneum.
• Parts of the lesser omentum :
– The hepatogastric ligaments
– The hepatoduodenal ligaments
• The stomach is connected to the:
– Inferior surface of the diaphragm by the gastrophrenic
ligament.
– Spleen by the gastrosplenic ligament (gastrolienal
ligament), which reflects to the hilum of the spleen.
– Transverse colon by the gastrocolic ligament, the
apron-like part of the greater omentum, which
descends from the greater curvature, turns under, and
then ascends to the transverse colon.
 Relations of the Stomach
• The two layers of the lesser omentum extend around the stomach
and leave its greater curvature as the greater omentum.
• The stomach is related to
– Anteriorly: the diaphragm, the left lobe of liver, and the anterior
abdominal wall.
– Posteriorly: most of the anterior wall of the omental bursa and the
pancreas; (Fig. 2.31A).
• The bed of the stomach:
– which the stomach rests in the supine position, is formed by the
structures forming the posterior wall of the omental bursa.
– From superior to inferior, the stomach bed is formed by the left dome
of the diaphragm, spleen, left kidney and suprarenal gland, splenic
artery, pancreas, and transverse mesocolon and colon (Fig. 2.31B).
 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.
 Artery of stomach
• The stomach has a rich arterial supply arising
from the celiac trunk and its branches.
• Anastomoses formed along the lesser curvature
by the right and left gastric arteries, and along
the greater curvature by the right and left gastro-
omental arteries.
• The fundus and upper body receive blood from
the short and posterior gastric arteries.
Arterial Supply to Stomach
 Rami Esophageales
A. Gastrica
sinistra
Cabang ke lambung
Arteriae gastrica
breves
Cabang-cabang ke
A. lienalis dalam lien
Truncus Arteria Gastro-
Celiacus omentalis sinistra
A.
Pancreaticoduodenalis
A. Gasroduodenalis superior
A. Gastro-omentalis
A. Hepatica dextra
communis Arteria gastrica dextra

A. Hepatica propria A. Hepatica sinistra

A. Hepatica dextra
 Veins of stomach
• The right and left gastric veins drain into the portal
vein
• The short gastric veins and left gastro-omental veins
drain into the splenic vein, which joins the superior
mesenteric vein (SMV) to form the portal vein.
• The right gastro-omental vein empties in the SMV.
• A prepyloric vein ascends over the pylorus to the right
gastric vein. Because this vein is obvious in living
persons, surgeons use it for identifying the pylorus.
Veins of stomach, duodenum, and spleen
 Lymphatic drainage of stomach
The gastric lymphatic vessels accompany the arteries along the greater
and lesser curvatures of the stomach. The following is a summary of
the lymphatic drainage of the stomach:
• Lymph from the superior two thirds of the stomach drains along the
right and left gastric vessels to the gastric lymph nodes; lymph
from the fundus and superior part of the body of the stomach also
drains along the short gastric arteries and left gastro-omental vessels
to the pancreatico-splenic lymph nodes.
• Lymph from the right two thirds of the inferior third of the stomach
drains along the right gastro-omental vessels to the pyloric lymph
nodes.
• Lymph from the left one third of the greater curvature drains along
the short gastric and splenic vessels to the pancreaticoduodenal
lymph nodes.
Lymphatic drainage of stomach
 Innervation of stomach
• The parasympathetic nerve supply of the
stomach is from the anterior and posterior vagal
trunks and their branches, which enter the
abdomen through the esophageal hiatus.
• The sympathetic nerve supply of the stomach
from the T6 through T9 segments of the spinal
cord passes to the celiac plexus through the
greater splanchnic nerve and is distributed
through the plexuses around the gastric and
gastro-omental arteries
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.
 Small Intestine
• The small intestine, consisting of the
duodenum, jejunum, and ileum, is the primary
site for absorption of nutrients from ingested
materials, and extends from the pylorus to the
ileocecal junction where the ileum joins the
cecum (the first part of the large intestine).
The pyloric part of the stomach empties into
the duodenum, duodenal admission being
regulated by the pylorus.
 DUODENUM
• The duodenum, the first and shortest (25 cm) part of the small
intestine, is also the widest and most fixed part.
• The duodenum pursues a C-shaped course around the head of the
pancreas.
• The duodenum begins at the pylorus and ends at the
duodenojejunal junction. This junction occurs approximately at
the level of the L2 vertebra, 2-3 cm to the right of the midline. The
junction usually takes the form of an acute angle, the
duodenojejunal flexure.
• Most of the duodenum is fixed by peritoneum to structures on the
posterior abdominal wall and is considered partially retroperitoneal.
• 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.
 Pars Superior Duodeni
• The first 2 cm of the superior part of the duodenum, immediately
distal to the pylorus, has a mesentery and is mobile. This free part,
called the ampulla (duodenal cap).
• The distal 3 cm of the superior part and the other three parts of the
duodenum have no mesentery and are immobile because they are
retroperitoneal.
• The superior part of the duodenum ascends from the pylorus and is
overlapped by the liver and gallbladder.
• Peritoneum covers its anterior aspect, but it is bare of peritoneum
posteriorly, except for the ampulla.
• The proximal part has the hepatoduodenal ligament (part of the
lesser omentum) attached superiorly and the greater omentum
attached inferiorly.
 Pars Descendens Duodeni
• The descending part of the duodenum runs inferiorly,
curving around the head of the pancreas.
• Initially, it lies to the right of and parallel to the IVC (inferior
vena cava).
• The bile and main pancreatic ducts enter its posteromedial
wall. These ducts usually unite to form the
hepatopancreatic ampulla, which opens on the summit of
an eminence, called the major duodenal papilla, located
posteromedially in the descending duodenum.
• The descending part of the duodenum is entirely
retroperitoneal.
 Pars Inferior (horizontal) Duodeni
• The inferior or horizontal part of the duodenum runs transversely to
the left, passing over the IVC, aorta, and L3 vertebra.
• It is crossed by the superior mesenteric artery and vein and the root
of the mesentery of the jejunum and ileum.
• Superior to it is the head of the pancreas and its uncinate process.
• The anterior surface of the horizontal part is covered with
peritoneum, except where it is crossed by the superior mesenteric
vessels and the root of the mesentery.
• Posteriorly it is separated from the vertebral column by the right
psoas major, IVC, aorta, and the right testicular or ovarian vessels.
 Pars Ascendens Duodeni
• The ascending part of the duodenum runs superiorly to reach the
inferior border of the body of the pancreas.
• Here it curves anteriorly to join the jejunum at the duodenojejunal
junction, supported by the attachment of a suspensory muscle of
the duodenum (ligament of Treitz).
• This muscle is composed of a slip of skeletal muscle from the
diaphragm and a fibromuscular band of smooth muscle from the
third and fourth parts of the duodenum.
• Contraction of this muscle widens the angle of the duodenojejunal
flexure, facilitating movement of the intestinal contents. The
suspensory muscle passes posterior to the pancreas and splenic
vein and anterior to the left renal vein.
 Artery of duodenum
• The arteries of the duodenum arise from the celiac trunk and the superior
mesenteric artery.
– The celiac trunk, via the gastroduodenal artery and its branch, the superior
pancreaticoduodenal artery, supplies the duodenum proximal to the entry of
the bile duct into the descending part of the duodenum.
– The superior mesenteric artery, through its branch, the inferior
pancreaticoduodenal artery, supplies the duodenum distal to the entry of the
bile duct.
• The pancreaticoduodenal arteries lie in the curve between the duodenum
and the head of the pancreas and supply both structures. The anastomosis
of the superior and inferior pancreaticoduodenal arteries, which occurs
approximately at the level of entry of the bile duct (or, according to some
authors, at the junction of the descending and horizontal parts of the
duodenum) is formed between the celiac and the superior mesenteric
arteries.
• An important transition in the blood supply of the
digestive tract occurs here:
– Proximally, extending orad (toward the mouth) to and
including the abdominal part of the esophagus, the blood
is supplied to the alimentary tract by the celiac trunk.
– Distally, extending aborad (away from the mouth) to the
left colic flexure, the blood is supplied by the SMA.
• The basis of this transition in blood supply is
embryological; this is the junction of the foregut and
midgut (Moore and Persaud, 2003).
Artery of duodenum
 Veins of duodenum
• The veins of the duodenum follow the arteries
and drain into the portal vein, some directly
and others indirectly, through the superior
mesenteric and splenic veins.
Veins of stomach, duodenum, and spleen
 Lymphatic drainage of duodenum
• The lymphatic vessels of the duodenum follow the
arteries.
– The anterior lymphatic vessels of the duodenum drain into
the pancreaticoduodenal lymph nodes, located along the
superior and inferior pancreaticoduodenal arteries, and
into the pyloric lymph nodes, which lie along the
gastroduodenal artery .
– The posterior lymphatic vessels pass posterior to the head
of the pancreas and drain into the superior mesenteric
lymph nodes.
• Efferent lymphatic vessels from the duodenal lymph
nodes drain into the celiac lymph nodes.
Lymphatic drainage of stomach
 Innervation of duodenum
• The nerves of the duodenum derive from the
vagus and greater and lesser
(abdominopelvic) splanchnic nerves by way
of the celiac and superior mesenteric
plexuses, from which they are conveyed to the
duodenum via periarterial plexuses extending
to the pancreaticoduodenal arteries.
HISTOLOGY OF GASTER AND
DUODENUM.
Esopaghus-cardia junction

http://eugraph.com/histology/digest/index.html
Stomach

http://histology-world.com/photoalbum/displayimage.php?album=26&pid=4276
Gaster
Histology of Cardia
Stomach

http://histologyatlas.wisc.edu/slides/382/labeled
Stomach

http://embryology.med.unsw.edu.au/embryology/images/f/ff/Stomach_histology_002.jpg
Pylorus – duodenum junction

http://www.siumed.edu/~dking2/erg/images/GI078b.jpg
Pylorus – duodenum junction

http://www.siumed.edu/~dking2/erg/images/GI075b.jpg
Duodenum
a. Lieberkhun gland
b. Tunica mucosa
c. Brunner gland
d. Tunica submucosa
e. Tunica muscularis
PHYSIOLOGY OF GASTER AND
DUODENUM
 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 (retropulsi)
 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
Control of gastric secretion
 Small Intestine
 The site where most digestion and absorbtion
take place.
 Divided into 3 segments: duodenum, jejunum
and ileum
 Its motility includes:
 Segmentation
 Migrating motility complex
 Segmentation
 Segmentation consists of oscillating, ring-like contraction of the
circular smooth muscle along the small intestine’s length; between
the contracted segments are relaxed areas containing a small bolus
of chyme.
 After a brief period of time, the contracted segments relax, and
ring-like contraction appear in the previously relaxed area.
 The new contraction forces the chyme in a previously relaxed
segment to move in both direction into the now relaxed adjacent
segments, shortly thereafter, the areas of contraction and
relaxation is alternate again.
 In this way, the chyme is chopped, churned and thoroughly mixed
 Functions: mixing the chyme with digestive juices secreted in
small-intestine lumen and exposing the chyme to the absorbtive
surface of the small intestines mucosa
Segmentation
 Migrating Motility Complex
 When most meal has been absorbed,
segmentation cease and are replaced
between meals by the migrating motility
complex.
 This between meal motility consists of weak,
repetitive peristaltic waves that move a short
distance down the intestine before dying out.
 Each contraction will sweep any remnants of
the preceding meal plus mucosal debris and
bacteria forward toward the colon
 Secretions
 Exocrine gland cells of small intestine mucosa
secrete about 1.5 liters of an aqueous salt and
mucus solution called succus entericus.
 Functions: provides protection and
lubrication also provides plenty of H2O to
participate in the digestion of food
 No digestive enzymes are secreted inti the
intestinal juice.
 Digestion
 Digestion within the small intestine lumen is
accomplished by pancreatic enzymes with fat
digestion being enhanced by bile secretion.
 This digestion is completed by special hairlike
projections of luminal surface of small instine
epithelial cell, microvilli
 Absorption
 All products of carbohydrate, protein and fat
digestion, as well as electrolytes, vitamin and
water are absorbed by small intestine
indiscriminately. Only absorption calcium and
iron is adjusted by body needs.
 Most absorption occurs in duodenum and
jejunum, very little in ileum (normally only
B12 and bile salt are absorbed by ileum)
BIOCHEMISTRY OF GASTER AND
DUODENUM.
TERMINOLOGY OF DYSPEPSIA
 DYSPEPSIA
• The description for a syndrome or collection
of symptoms / complaints of pain or
discomfort in regio epigatrica, bloating,
nausea, vomiting, belching, quickly feeling full,
stomach feel full.
 ETIOLOGY
• Disorders or diseases in the lumen of the
digestive tract
• Drugs
• Diseases of the liver, pancreatic, biliary system
• Systemic diseases
 Sign & Symptom
• The characteristic symptoms of dyspepsia are
– upper abdominal pain,
– bloating,
– fullness and tenderness on palpation.
– nausea
 Diagnose
• Full blood count and erythrocyte sedimentation
rate
• The x-ray tests include:
– The upper gastrointestinal series
– The small bowel series
– The barium enema
– CT scan
• The endoscopic tests include:
– EGD
– Colonoscopy
Diagnostic Criteria ROME III
 Treatment
• Antacids
• Anticholinergics
• Prokinetik
• Sitoprotektif
• Histamine H2 Antagonist
GERD (GASTROESOFAGAL
REFLUX DISEASES)
 GERD
• Gastroesophageal reflux disease (GERD) is a condition
in which food or liquid travels backwards from the
stomach to the esophagus (the tube from the mouth to
the stomach).
• Occurs when the amount of gastric juice that refluxes
into the esophagus exceeds the normal limit, causing
symptoms with or without associated esophageal
mucosal injury
• This action can irritate the esophagus, causing
heartburn and other symptoms.
• Gastroesophageal reflux is a common condition that
often occurs without symptoms after meals.
 Classification
Gastroesophageal Reflux

Physiological Gastroesophageal Gastroesophageal Reflux

Reflux - GER Disease – GERD
(Symptomatic)

Primary GERD: Secondary GERD:

Motility problem External factor causing transient
Affecting lower relaxations of lower Esophageal
Esophageal sphincter sphincter (eg. Food allergy)
Gastroesophageal Reflux Disease
(GERD)
 Etiology
• Lifestyle - Use of alcohol or cigarettes, obesity, poor
posture (slouching)
• Medications - Calcium channel blockers, theophylline,
nitrates, antihistamines
• Diet - Fatty and fried foods, chocolate, garlic and
onions, drinks with caffeine, acid foods such as citrus
fruits and tomatoes, spicy foods, mint flavorings
• Eating habits - Eating large meals, eating soon before
bedtime
• Other medical conditions - Hiatal hernia, pregnancy,
diabetes, rapid weight gain
 Gastroesophageal Reflux
Pathophysiology
Swallow

The lower esophageal sphincter relaxes or

Decrease the pressure of the LES or
Increased intra-abdominal pressure

Stomach contents and corrosive acid well up

Regurgitation

Damage the lining of the esophagus

 GERD – Treatment
• Lifestyle changes
– dietary modifications (avoid acidic / reflux-
inducing foods (tomatoes, chocolate, mint), &
beverages (juices, carbonated, caffeinated drinks,
alcohol), altered sleep position, weigh reduction,
smoking cessation
• Pharmacotherapy
• Surgical therapies
Treatment – Pharmacotherapy
 Examination
• Bernstein test
• Barium meal test
• Endoscopy
• Ph
• Ppi test
GASTRITIS
 GASTRITIS
• Gastritis is an inflammation, irritation, or
erosion of the lining of the stomach / gastric
mucosa. It can occur suddenly (acute) or
gradually (chronic).

RISK FACTOR OF GASTRITIS

 H. pylori infection
 Regular use of aspirin or other NSAIDs
 Older age
 ETIOLOGY OF GASTRITIS
• Bacterial infection
• Regular use of pain relievers
• Excessive alcohol use
• Stress
• Bile reflux disease
• Your own body attacking cells in your stomach
(autoimmune gastritis)
• Other diseases and conditions
 CLASSIFICATION OF GASTRITIS
• Acute gastritis
– Acute H. pylori infection
– Other acute infectious gastritis
• Chronic atrophic gastritis
– Type A
– Type B
– Indeterminant
• Uncommon forms of gastritis
– Lymphocytic
– Eosinophilic
– Crohn’s disease
– Sarcoidosis
– Isolated granulomatous gastritis
 SYMPTOMS OF GASTRITIS
• Nausea or recurrent upset stomach
• Abdominal bloating
• Abdominal pain
• Vomiting
• Indigestion
• Burning or gnawing feeling in the stomach
between meals or at night
• Vomiting blood or coffee ground-like material
• Black, tarry stools
 Infection of H. PILORY

gastritis TH 1 motility
H.Pylory
infects gaster
urease
protective TH2
Vac A Urea
ammonia
+CO2
Provides a survival needs for bacteria
Causes epithelial injury
 Pathogenesis of Helicobacter pylori infection

• An ability to colonize and adhere to gastric

epithelial cells.
• The possesion of flagella that allows movement
through the luminal mucous layer to site of higher
Ph.
• An ability of adherent strains to supress acid
secretion to improve their survival.
• Secretion of urease that produces ammonia
results in a more alkaline environment.
• Release of vacuolating cytotoxin (VacA) that
promotes bacterial survival and causes epithelial
injury.
• The presence of cytotoxin-assosiated gene (CagA) strains that can escape
normal immune responses and cause inflammation with release of
inflammatory cytokines and reactive oxygen metabolites that damages
mucosal epitelial cells and loss of the protective mucosal barrier.
• Recruitment and activation of neutrophils,macrophages,and mast cells
with release of inflammatory cytokines that promote celllar injury.
• Down-regulation of antral somatostatin leading to increased
gastrin,acid,impaired mucosal bicarbonat production and increased
mucosal exposure to acid and pepsin.
• Activation/inhibition of T-and B- cell immune
responses that may contribute to mucosal
injury.
• Release of cytokines and chemokines that
promote gastric epithelial cell death and cell
proliferation that can result in
atrophy,ulcers,or malignant growth.
 Examination
• Urea breath test
• Serologi
• Biopsy urea test
• Manifestacion:
– Burn feeling (in epigastrium)
– Nausea
– Bitter in the tounge
– Disfagia

Complication:
Esophagitis is classified into the following 4
gradesI,II,III,IV.
PEPTIC ULCER
 Peptic ulcer
• Open sores that develop on the inside lining of
your stomach, upper small intestine or
esophagus.
• The most common symptom of a peptic ulcer
is abdominal pain
• The two most common types of peptic ulcer
are called “gastric ulcers” and “duodenal
ulcers”
 What causes peptic ulcers?
• A bacterium called Helicobacter pylori
• Nonsteroidal anti-inflammatory drugs.
• Rarely, cancerous or noncancerous tumors in the
stomach, duodenum, or pancreas cause ulcers.
• Drinking too much alcohol
• Smoking cigarettes or chewing tobacco
• Radiation treatments

Peptic ulcers are not caused by stress or eating spicy food, but both can make
ulcer symptoms worse. Smoking and drinking alcohol also can worsen ulcers
and prevent healing.
 patofisiologi
H. Pylori Urease Netralisir asam lambung
Mucin B + Antibodi tubuh ↑
phospolipase Peradangan sel mukosa lambung

H.Pylori kolonisasi

Nembus cairan lambung

+
Nempel sel epitel

H. Kolonisasi GU
+
Nempel di epitel duodenal
reflux
PUD DU
What are the symptoms of a peptic
ulcer?
• Abdominal discomfort
• Felt anywhere between the
navel and the breastbone, this
discomfort usually
• Other symptoms include
– weight loss
– poor appetite
– bloating
– burping
– nausea
– vomiting
 What are the symptoms of a peptic
ulcer?
• Emergency Symptoms
– sharp, sudden, persistent, and severe stomach pain
– bloody or black stools
– bloody vomit or vomit that looks like coffee grounds

• “alarm” symptoms could be signs of a serious problem

– bleeding—when acid or the peptic ulcer breaks a blood vessel
– perforation—when the peptic ulcer burrows completely through
the stomach or duodenal wall
– obstruction—when the peptic ulcer blocks the path of food
trying to leave the stomach
 How are ulcers diagnosed?
• upper GI series
• EGD
 Treatment
• If you have a peptic ulcer with an H. pylori infection, the standard treatment uses different
combinations of the following medications for 5 - 14 days:
– Two different antibiotics to kill H. pylori, such as clarithromycin (Biaxin), amoxicillin,
tetracycline, or metronidazole (Flagyl)
– Proton pump inhibitors such as omeprazole (Prilosec), lansoprazole (Prevacid), or
esomeprazole (Nexium)
– Bismuth (the main ingredient in Pepto-Bismol) may be added to help kill the bacteria

• If you have an ulcer without an H. pylori infection, or one that is caused by taking aspirin or NSAIDs,
your doctor will likely prescribe a proton pump inhibitor for 8 weeks.

• Other medications that may be used for ulcer symptoms or disease are:
– Misoprostol, a drug that may help prevent ulcers in people who take NSAIDs on a regular basis
– Medications that protect the tissue lining (such as sucralfate)
 Possible Complications
• Bleeding inside the body (internal bleeding)
• Gastric outlet obstruction
• Inflammation of the tissue that lines the wall
of the abdomen (peritonitis)
• Perforation of the stomach and intestines
 References
• Dalley, Arthur F. Keith L Moore. Clinically Oriented Anatomy.
5th edition. Lippincott Williams & Wilcins; 2006
• Fauci, Braunwald, Kasper, dkk. Harrison’s Principles of Internal
Medicine vol II. Ed 17.United Stated : mcGraw-Hills, 2008.