Problem 2B(child)

Stephen Wijayanto
405110198
Faculty of Medicine
Tarumanagara University
Group 09 - Gastrointestinal system block
 Problem 2b
A 10 years old girl has lost her appetite and
complains of nausea, copious vomiting and bloating
since 2 moths ago. Her stool consistency sometimes
unformed and watery. The girl likes to eat ‘instant
noodle’ and ‘hot spicy food’. For medication history:
she usually has paracetamol if getting fever.
Physical examination showed epigastric pain,
increasing peristaltic, and tympanic sound on
abdominal percussion.
What can you learn from the problem?
 Step 1
Unfamiliar Terms
----
 Step 2
Problems
1. Is there any relation between patient’s
compliments and her eating behaviour?
2. Why her stool consistency unformed and
watery ?
3. is there any relation between paracetamol
and her symptom?
4. Interpretation of physical assessment!
 Step3
Brainstorming
1. A. Because hot spicy food is able to irritate
intestinal villigastroenteritis
B. Because instant noodle flavors contain much
Natrium  increasing gastric juice
2. Hot spicy food is able to irritate intestinal villi 
gastroenteritis  reduce the water reabsorption
3. There is no relation between paracetamol usage
with epigastric pain symptoms
4. A. Epigastric pain in upper GIT
B. ↑peristaltic  ↑ HCl  ↑peristaltic
C. Normal tympanic sound
 Step 4
Mind Map
Girl 10 year
old

Complaint:
Lifestyle: Examination:
a. Lost of appetite
a. Eating instant noodle a. Epigastric pain
b. Nausea
b. Eating hot spicy food b. ↑peristaltic
c. Copious vomiting
c. Using paracetamol if c. Suara timpanik (perkusi)
d. Bloat
getting fever
e. Unformed and watery
feces

Alarm Nausea Vomit

GERD NSAID dyspepsia symptom
 Step 5
Learning Objective
1. Anatomy, Histology, Physiology, and
Biochemistry of gaster, duodenum, jejunum,
and ileum
2. Terminology of dyspepsia
3. Terminology of GERD
Anatomy , Histology, Physiology, and
Biochemistry of gaster, duodenum, jejunum,
ileum.

LO1.
 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.
 Parts of the Stomach
The stomach has four parts (Fig. 2.30A):
• Cardia: the part surrounding the cardial orifice.
• Fundus: the dilated superior part that is related to the left dome of the
diaphragm and is limited inferiorly by the horizontal plane of the cardial
orifice. The superior part of the fundus usually reaches the level of the left
5th intercostal space. The cardial notch (cardial incisure) is between the
esophagus and the fundus. The fundus may be dilated by gas, fluid, food,
or any combination of these.
• Body (corpus): the major part of the stomach between the fundus and the
pyloric antrum.
• Pyloric part: the funnel-shaped outflow region of the stomach; its wide
part, the pyloric antrum, leads into the pyloric canal, its narrow part. The
pylorus (G. gatekeeper), the distal, sphincteric region of the pyloric part, is
a marked thickening of the circular layer of smooth muscle, which controls
discharge of the stomach contents through the pyloric orifice into the
duodenum.
 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 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.
The muscle layers of the oesophageal
and gastric walls
 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.
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. 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
• 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.
JEJUNUM - ILEUM
• Jejunum
– begins at the
duodenojejunal flexure
where the alimentary
tract resumes an
intraperitoneal course
• Ileum
– ends at the ileocecal
junction, the union of
the terminal ileum and
the cecum
 Artery of Jejunum-Ileum
• The superior mesenteric artery supplies the
jejunum and ileum.
• The SMA usually arises from the abdominal aorta
at the level of the L1 vertebra, approximately 1
cm inferior to the celiac trunk, and runs between
the layers of the mesentery, sending 15-18
branches to the jejunum and ileum.
• The arteries unite to form loops or arches, called
arterial arcades, which give rise to straight
arteries, called vasa recta.
 Veins of Jejunum-Ileum
• The superior mesenteric vein drains the
jejunum and ileum. It lies anterior and to the
right of the SMA in the root of the mesentery.
The SMV ends posterior to the neck of the
pancreas, where it unites with the splenic vein
to form the portal vein.
 Lymphatic drainage of Jejunum-Ileum
• Specialized lymphatic vessels in the intestinal villi (tiny projections
of the mucous membrane) that absorb fat are called lacteals.
• They empty their milk-like fluid into the lymphatic plexuses in the
walls of the jejunum and ileum. The lacteals drain in turn into
lymphatic vessels between the layers of the mesentery. Within the
mesentery, the lymph passes sequentially through three groups of
lymph nodes:
– Juxta-intestinal lymph nodes: located close to the intestinal wall.
– Mesenteric lymph nodes: scattered among the arterial arcades.
– Superior central nodes: located along the proximal part of the SMA.
• Efferent lymphatic vessels from the mesenteric lymph nodes drain
to the superior mesenteric lymph nodes. Lymphatic vessels from the
terminal ileum follow the ileal branch of the ileocolic artery to the
ileocolic lymph nodes.
 Innervation of Jejunum-Ileum
• The SMA and its branches are surrounded by a perivascular nerve plexus
through which the nerves are conducted to the parts of the intestine
supplied by this artery.
• The sympathetic fibers in the nerves to the jejunum and ileum originate in
the T8-T10 segments of the spinal cord and reach the superior
mesenteric nerve plexus through the sympathetic trunks and thoracic
abdominopelvic (greater, lesser, and least) splanchnic nerves.
• The presynaptic sympathetic fibers synapse on cell bodies of postsynaptic
sympathetic neurons in the celiac and superior mesenteric (prevertebral)
ganglia.
• The parasympathetic fibers in the nerves to the jejunum and ileum derive
from the posterior vagal trunks.
• The presynaptic parasympathetic fibers synapse with postsynaptic
parasympathetic neurons in the myenteric and submucosal plexuses in the
intestinal wall.
HISTOLOGY OF GASTER AND
DUODENUM.
Gaster
Histology of Cardia
Duodenum
a. Lieberkhun gland
b. Tunica mucosa
c. Brunner gland
d. Tunica submucosa
e. Tunica muscularis
Jejunum
a. Villi
b. Plica kerckringi
c. Tunica muscularis
mucosa
d. Tunica submucosa
e. Tunica muscularis
Ileum
a. Villi
b. Lymphonodus aggregati
c. Tunica muscularis
mucosa
d. Tunica submucosa
e. Tunica muscularis
a. Liberkhun gland
b. Goblet cell
c. Paneth cell
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
 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.
LO2. 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
HEARTBURN
 Heartburn
• Is a burning feeling in the lower chest, along
with a sour or bitter taste in the throat and
mouth
 What causes heartburn?
• Food passes from your mouth to esophagus
through Lower Esophagus Sphincter (LES).
• Usually, LES closes as soon as food passes
through. But if it doesn't close all the way 
acid from your stomach can get through the
opening and into your esophagus(reflux).
• Stomach acid can irritate the esophagus and
cause heartburn.
Things that can make heartburn worse
• Cigarette smoking • Onions
• Coffee / Caffein • Lying down too soon
• Alcohol after eating
• Carbonated drinks • Being overweight or
• Citrus fruits obese
• Chocolate, mints or • Aspirin or ibuprofen
peppermints • Certain medicines
 Can heartburn be serious?
If you get more than occasional heartburn, it
may be a symptom of:
• acid reflux disease, gastroesophageal reflux
disease (GERD),
• an inflamed stomach lining (gastritis),
• hiatal hernia
• peptic ulcer.
 Tips on preventing heartburn
• Try to eat at least 2 to 3 hours before lying down.
If you take naps, try sleeping in a chair.
• Don’t smoke
• Lose weight if you're overweight.
• Don't overeat.
• Eat high-protein, low-fat meals.
• Avoid tight clothes
• Avoid foods and other things that give you
heartburn
ABDOMINAL BLOATING
 Abdominal bloating
• a condition in which the abdomen (belly) feels
full and tight. The abdomen may be visibly
swollen (distended).
 Causes
• Common causes include:
– Air swallowing (a nervous habit)
– Constipation
– Gastroesophageal reflux
– Irritable bowel syndrome
– Lactose intolerance and other food intolerances
– Overeating
– Small bowel bacterial overgrowth
– Weight gain
More serious disorders that may cause
bloating are:
• Ascites and tumors
• Celiac disease
• Dumping syndrome
• Ovarian cancer
• When the pancreas is not able to produce enzymes to help
digestion (pancreatic insufficiency)
 Home Care
– Avoid chewing gum or carbonated drinks,
especially those with high levels of fructose or
sorbitol
– Avoid foods such as Brussels sprouts, turnips,
cabbage, beans, and lentils
– Do not eat too quickly
– Stop smoking
– Treat your constipation, with fiber supplements
such as psyllium can make your symptoms worse.
 When to contact a medical
professional
• Call your health care provider if you have:
– Abdominal pain
– Blood in the stools or dark, tarry looking stools
– Diarrhea
– Heartburn that is getting worse
– Vomiting
– Weight loss
NAUSEA & VOMITING
 Mechanism of Nausea and Vomiting

• Vomit
– Expulsion with persistent of stomach contents out from
mouth,commonly it’s consider cause by abnormal gastric motility.
– Vomit doesn’t appear by reverse peristaltic.
– The most important force that press gastric contents such as
diaphragm contraction(priory inspiration muscle) and abdominal
muscle (active extrinsic muscle)
• Nausea is the sensation of having an urge to vomit.
• Vomit is start with:
– Inhale and glottis closingcontraction of
diaphragm descend to press gastric and
abdominal muscle’s contraction press abdomen
cavityintraabdomen pressure (↑) and abdomen
contents pushed to the top gastric pushed from
top and under gastric contents push to in
oesophagus and out from mouth.
• Glottis closingvomit didn’t enter to
resporatory tract.
• Uvula was liftedclose a nasal cavity.
• Vomit a yellow appearancethere’s a gall
that enter to duodenum from hepar and gall
bladder.
• Usually,vomit was started by many common
sign:
– Expulsion of saliva >>>
– Sweating
– Heartbeats velocity (↑)
– Nausea
 Etiology of vomit
• Tactil stimulation on larynx’s backside.
• Iritation on stomach or duodenum
• Intracranial pressure (↑)ex/ intercerebrum bleeding
• Rotation or head accelerationdizzy ex/
carsick/seasick/airsick
• Intensive pain from another organ
• Chemicalex emetic drugs
• Pshycis vomit (by emotion factor)
• Vomit >>>body will get liquid and acid
expulsion that was reabsorption on normal
condition.
• Plasma volume decreasedwill get
dehidration and circulation problems
• Acid is outmetabolic alcalosis.
 Management
• Identification and elimination of the
underlying cause if possible
• Control of the symptoms if it is not possible to
eliminate the underlying cause
• Correction of electrolyte, fluid or nutritional
deficiencies
 Diagnostic
• Blood tests
• Urinalysis
• X-rays of the abdomen
 Treatment
• Give intravenous fluids.
If dehydration is severe
• Antivomiting drugs (anti-emetics)
may be helpful but they should be used only
when the potential benefits outweigh the
risks.
LO3. GERD
 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)
Epidemiology
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.