Problem 2A (Adult)

Frudensia Kristiana
405110031
Faculty of Medicine
Tarumanagara University
Group 16 -

Learning Objectives:
1. Able to know and explain about anatomy
2.
3.
4.
5.

of gaster, duodenum, jejunum, ileum.

Able to know and explain about histology
of gaster and duodenum.
Able to know and explain about physiology
of gaster and duodenum.
Able to know and explain about
biochemistry of gaster and duodenum.
Able to know and explain about dyspepsia.

LO1.
Anatomy of gaster, duodenum,
jejunum, ileum.

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

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 (710 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 JejunumIleum

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.

LO2.
Histology of gaster and duodenum.

Gaster

Histology of Cardia

Duodenum
a.
b.
c.
d.
e.

Lieberkhun gland
Tunica mucosa
Brunner gland
Tunica submucosa
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

LO3.
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
Stomachs mixing movement ingested
food pulverized & mixed with gastric
secretions thick liquid mixture (chyme)
Gastrics 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

Pepsins autocatalytic activity

Mucus
Lubricating properties, protects gastric

mucosa
Protect the stomach wall from self-digestion
because of pepsin
doesnt affect pepsin activity in the lumen

Being alkaline neutralizing HCl

Doesnt 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 intestines 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

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

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

LO4.
Biochemistry of gaster and
duodenum.

LO5.
DYSPEPSIA

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

Alcohol

soon after eating

Being overweight
or obese
Aspirin or ibuprofen
Certain medicines

Carbonated drinks
Citrus fruits
Chocolate, mints or

peppermints

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.
Dont 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 its consider cause by

abnormal gastric motility.
Vomit doesnt 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 closingcontraction of

diaphragm descend to press gastric and

abdominal muscles contraction press
abdomen cavityintraabdomen 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 closingvomit didnt enter to

resporatory tract.
Uvula was liftedclose a nasal cavity.
Vomit a yellow appearancetheres 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 larynxs backside.
Iritation on stomach or duodenum
Intracranial pressure ()ex/ intercerebrum

bleeding
Rotation or head accelerationdizzy ex/
carsick/seasick/airsick
Intensive pain from another organ
Chemicalex emetic drugs
Pshycis vomit (by emotion factor)

Vomit >>>body will get liquid and acid

expulsion that was reabsorption on normal

condition.
Plasma volume decreasedwill get
dehidration and circulation problems
Acid is outmetabolic 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.

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 Reflux GER

Primary GERD:
Motility problem
Affecting lower
Esophageal sphincter

Gastroesophageal Reflux
Disease GERD
(Symptomatic)

Secondary GERD:
External factor causing
transient relaxations of
lower Esophageal 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
Crohns 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
H.Pylory
infects
gaster

protective TH2

motility

urease

Vac A
Provides a survival needs for bacteria
Causes epithelial injury

Urea
ammoni
a +CO2

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
gradesI,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
Mucin B
phospolipase

Netralisir asam lambung

Antibodi tubuh
+
Peradangan sel mukosa lambung

H.Pylori kolonisas

Nembus cairan lambu

+
Nempel sel epitel
H. Kolonisasi
+
Nempel di epitel
PUD

DU

GU
reflux

duodenal

What are the symptoms of a

peptic ulcer?

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

bleedingwhen acid or the peptic ulcer breaks a

blood vessel
perforationwhen the peptic ulcer burrows
completely through the stomach or duodenal wall
obstructionwhen 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. Harrisons
Principles of Internal Medicine vol II. Ed
17.United Stated : mcGraw-Hills, 2008.