BY: VARLA S.

G (405090215)
PROBLEM 1A
ANATOMY OF DIGESTIVE
TRACT
Embryology
Part

Range in
adult
Gives rise to Arterial
supply
Foregut The pharynx,
to the upper
duodenum
Pharynx, esophagus, stomach, upper
duodenum, respiratory tract (including
the lungs), liver, gallbladder, and
pancreas
Branches of
the celiac
artery
Midgut Lower
duodenum, to
the first half of
the transverse
colon
Lower duodenum, jejunum, ileum,
cecum, appendix, ascending colon,
and first half of the transverse colon
Branches of
the superior
mesenteric
artery
Hindgut Second half of
the transverse
colon, to the
upper part of
the anal canal
Remaining half of the transverse
colon, descending colon, rectum, and
upper part of the anal canal
Branches of
the inferior
mesenteric
artery
PHYSIOLOGY OF DIGESTIVE
TRACT

The functions of the digestive system are:
Ingestion - eating food
Digestion - breakdown of the food
Absorption - extraction of nutrients from
the food
Defecation - removal of waste products
The digestive system is a group of organs that
breakdown the chemical components of food, with
digestive juices, into micromolecul nutrients which
can be absorbed to generate energy for the body

The bucal cavity (mouth) and salivary
glands
Food enters the mouth and is chewed by the teeth,
turned over and mixed with saliva by the tongue.
Mouth: the salivary glands. Saliva produced by these
glands contains an enzyme that begins to digest the
starch from food into smaller molecules. ptyalin
enzyme
The Stomach
It is the widest part of the alimentary canal
and acts as a reservoir for the food where it
may remain for between 2 and 6 hours.
Here the food is churned over and mixed with
various hormones, enzymes including
pepsinogen which begins the digestion of
protein, hydrochloric acid, and other
chemicals
The stomach has an average capacity of 1
liter, varies in shape, and is capable of
considerable distension.
At regular intervals a circular muscle at the
lower end of the stomach, the pylorus opens
allowing small amounts of food, now known
as chyme to enter the small intestine.

Duodenum
Small Intestine
The small intestine measures about 7m in an
average adult and consists of the duodenum,
jejunum, and ileum.
Both the bile and pancreatic ducts open into
the duodenum together.
The small intestine, because of its structure,
provides a vast lining through which further
absorption takes place.
The Large Intestine
The large intestine averages about 1.5m long
and comprises the caecum, appendix, colon,
and rectum.
Here most of the water and electrolytes is
absorbed, much of which was not ingested,
but secreted by digestive glands further up the
digestive tract.
The colon is divided into the ascending,
transverse and descending colons, before
reaching the anal canal where the indigestible
foods are expelled from the body.
Picture : process of swallowing
PEPTIC ULCER
DEFINITION
Peptic ulcers are open sores that develop on the
inside lining of stomach and the upper portion of
small intestine.
The most common symptom of a peptic ulcer is
abdominal pain
Peptic ulcers that occur on the inside of the
stomach are called gastric ulcers.
Peptic ulcers that affect the inside of the upper
portion of small intestine (duodenum) are called
duodenal ulcers.


Gross pathology of a gastric ulcer.
EPIDEMIOLOGY
United States statistics
In the United States, PUD affects approximately 4.5
million people annually. Only about 10% of young
persons have H pylori infection; the proportion of
people with the infection increases steadily with
age.
Overall, the incidence of duodenal ulcers has been
decreasing over the past 3-4 decades.
The prevalence of PUD has shifted from
predominance in males to similar occurrences in
males and females
International statistics
The frequency of PUD in other countries is variable
and is determined primarily by association with the
major causes of PUD: H pylori and NSAIDs.


ETIOLOGY
Normally, the lining of the stomach and small
intestines are protected against the irritating acids
produced in stomach. If this protective lining
stops working correctly, and the lining breaks
down, it results in inflammation (gastritis) or an
ulcer.
Most ulcers occur in the first layer of the inner
lining. A hole that goes all the way through the
stomach or duodenum is called a perforation. A
perforation is a medical emergency.
The most common cause of such damage is
infection of the stomach by bacteria
called Helicobacter pylori (H.pylori). Most people
with peptic ulcers have these bacteria living in
their gastrointestinal (GI) tract.
ADDITIONAL ETIOLOGIC
FACTORS
Hepatic cirrhosis
Chronic obstructive pulmonary
disease
Allergic gastritis and eosinophilic
gastritis
Cytomegalovirus infection
Graft versus host disease
Uremic gastropathy
Henoch-Schnlein gastritis
Corrosive gastropathy
Celiac disease
Bile gastropathy
Autoimmune disease
Crohn disease
Other granulomatous gastritides
(eg, sarcoidosis, histiocytosis
X,tuberculosis)
Phlegmonous gastritis and
emphysematous gastritis
Other infections, including
Epstein-Barr virus,
HIV, Helicobacter
heilmannii, herpes
simplex, influenza, syphilis, Candi
da
albicans,histoplasmosis, mucormy
cosis, and anisakiasis
Chemotherapeutic agents, such
as 5-fluorouracil (5-FU),
methotrexate (MTX), and
cyclophosphamide
Local radiation resulting in
mucosal damage, which may lead
to the development of duodenal
ulcers
Use of crack cocaine, which
causes localized vasoconstriction,
resulting in reduced blood flow
and possibly leading to mucosal
damage

PATOPHYSIOLOGY
Peptic ulcers are defects in the gastric or duodenal
mucosa that extend through the muscularis mucosa.
The epithelial cells of the stomach and duodenum
secrete mucus in response to irritation of the epithelial
lining and as a result of cholinergic stimulation.
The superficial portion of the gastric and duodenal
mucosa exists in the form of a gel layer, which is
impermeable to acid and pepsin.
Other gastric and duodenal cells secrete bicarbonate,
which aids in buffering acid that lies near the mucosa.
Prostaglandins of the E type (PGE) have an important
protective role, because PGE increases the
production of both bicarbonate and the mucous layer.
Under normal conditions, a physiologic balance
exists between gastric acid secretion and
gastroduodenal mucosal defense.
Mucosal injury and, thus, peptic ulcer occur when
the balance between the aggressive factors and
the defensive mechanisms is disrupted.
Aggressive factors, such as NSAIDs, H
pylori infection, alcohol, bile salts, acid, and
pepsin, can alter the mucosal defense by allowing
back diffusion of hydrogen ions and subsequent
epithelial cell injury.
The defensive mechanisms include tight
intercellular junctions, mucus, mucosal blood flow,
cellular restitution, and epithelial renewal.
When H pylori colonizes the gastric mucosa,
inflammation usually results.
In patients infected with H pylori, high levels of
gastrin and pepsinogen and reduced levels of
somatostatin have been measured.
In infected patients, exposure of the duodenum to
acid is increased.
Virulence factors produced by H pylori,including
urease, catalase, vacuolating cytotoxin, and
lipopolysaccharide, are well described.
Most patients with duodenal ulcers have impaired
duodenal bicarbonate secretion, which has also
proven to be caused by H pylori because its
eradication reverses the defect

.
The combination of increased gastric acid
secretion and reduced duodenal bicarbonate
secretion lowers the pH in the duodenum, which
promotes the development of gastric metaplasia
(ie, the presence of gastric epithelium in the first
portion of the duodenum). H pylori infection in
areas of gastric metaplasia induces duodenitis
and enhances the susceptibility to acid injury,
thereby predisposing to duodenal ulcers.
RISK FACTORS
Drinking too much alcohol
Regular use of aspirin, ibuprofen, naproxen, or other
nonsteroidal anti-inflammatory drugs (NSAIDs).
Taking aspirin or NSAIDs once in awhile is safe for
most people.
Smoking cigarettes or chewing tobacco
Being very ill, such as being on a breathing machine
Radiation treatments
A rare condition called Zollinger-Ellison
syndrome causes stomach and duodenal ulcers.
Persons with this disease have a tumor in the
pancreas that releases high levels of a hormone,
which causes an increase in stomach acid.
Many people believe that stress causes ulcers. It is
not clear if this is true, at least for everyday stress at
home.


SYMPTOMS
Small ulcers may not cause any symptoms. Some ulcers
can cause serious bleeding.
Abdominal pain is a common symptom but it doesn't
always occur. The pain can differ a lot from person to
person.
Feeling of fullness -- unable to drink as much fluid
Hunger and an empty feeling in the stomach, often 1 - 3 hours
after a meal
Mild nausea (vomiting may relieve symptom)
Pain or discomfort in the upper abdomen
Upper abdominal pain that wakes you up at night
Other possible symptoms include:
Bloody or dark tarry stools
Chest pain
Fatigue
Vomiting, possibly bloody
Weight loss

PHYSICAL EXAMINATION
In uncomplicated PUD, the clinical findings are few and
nonspecific and include the following:
Epigastric tenderness (usually mild)
Guaiac-positive stool resulting from occult blood loss
Melena resulting from acute or subacute gastrointestinal
bleeding
Succussion splash resulting from partial or complete gastric
outlet obstruction
Patients with perforated PUD usually present with a
sudden onset of severe, sharp abdominal pain.
Most patients describe generalized pain; a few present
with severe epigastric pain. As even slight movement can
tremendously worsen their pain, these patients assume a
fetal position.
Abdominal examination usually discloses generalized
tenderness, rebound tenderness, guarding, and rigidity.
However, the degree of peritoneal findings is strongly
influenced by a number of factors, including the size of
perforation, amount of bacterial and gastric contents
contaminating the abdominal cavity, time between
perforation and presentation, and spontaneous sealing of
perforation.
These patients may also demonstrate signs and symptoms
of septic shock, such as tachycardia, hypotension, and
anuria.


SIGNS AND TESTS
Esophagogastroduodenoscopy (EGD) is a
special test performed by a gastroenterologist in
which a thin tube with a camera on the end is
inserted through your mouth into the GI tract to
see your stomach and small intestine. During an
EGD, the doctor may take a biopsy from the wall
of your stomach to test for H. pylori.
Upper GI is a series of x-rays taken after you
drink a thick substance called barium.
Other tests:
Hemoglobin blood test to check for anemia
Stool guaiac to test for blood in your stool

Angiography
Angiography may be necessary in patients with a massive GI
bleed in whom endoscopy cannot be performed. An ongoing
bleeding rate of 0.5 mL/min or more is needed for the
angiography to be able to accurately identify the bleeding source.
Angiography can depict the source of the bleeding and can help
provide needed therapy in the form of a direct injection of
vasoconstrictive agents.
Serum Gastrin Level
A fasting serum gastrin level should be obtained in certain cases
to screen for Zollinger-Ellison syndrome. Such cases include the
following:
Patients with multiple ulcers
Ulcers occurring distal to the duodenal bulb
Strong family history of PUD
Peptic ulcer associated with diarrhea, steatorrhea, or weight loss
Peptic ulcer not associated with H pylori infection or NSAID use
Peptic ulcer associated with hypercalcemia or renal stones
Ulcer refractory to medical therapy
Ulcer recurring after surgery
Secretin Stimulation Test
A secretin stimulation test may be required if the diagnosis of
Zollinger-Ellison syndrome cannot be made on the basis of the
serum gastrin level alone. This test can distinguish Zollinger-
Ellison syndrome from other conditions with a high serum gastrin
level, such as use of antisecretory therapy with a proton pump
inhibitor, renal failure, or gastric outlet obstruction.
Biopsy
A single biopsy offers 70% accuracy in diagnosing gastric cancer,
but 7 biopsy samples obtained from the base and ulcer margins
increase the sensitivity to 99%. Brush cytology has been shown
to increase the biopsy yield, and this method may be useful
particularly when bleeding is a concern in a patient with
coagulopathy.
Histologic Findings
The histology of gastric ulcer depends on its chronicity. The
surface is covered with slough and inflammatory debris. Beneath
this neutrophilic infiltration, active granulation with mononuclear
leukocytic infiltration and fibrinoid necrosis may be seen. In
chronic superficial gastritis, lymphocytes, monocytes, and plasma
cells often infiltrate the mucosa and submucosa.
Emergency department workup
The ED workup will vary depending on presentation and includes
the following:
Complete blood count is used to evaluate acute or chronic blood loss.
Electrolytes, BUN, and creatinine levels are useful tests for critical-
appearing patients who require fluid resuscitation.
Type and screen and crossmatched blood for transfusion is indicated in
unstable or potentially critical patients.
aPTT, PT, and INR are indicated in patients with active bleeding and those
on anticoagulants.
Amylase, lipase, and liver transaminase levels can be helpful to rule out
other common causes of epigastric pain.
Patients younger than 55 years with no alarm features should be referred
for noninvasive testing for H pylori infection in the outpatient setting.
[1]


Gastric ulcer with punched-out ulcer base with whitish
fibrinoid exudates
Gastric ulcer (lesser curvature) with punched-out ulcer base with whitish
exudate
Gastric cancer. Note the irregular heaped up overhanging
margins
Gastric cancer with ulcerated
mass
Duodenal ulcer in a 35-year-old woman who presented with tarry stools and a hemoglobin
level of 75 g/L.
Duodenal ulcer in a 65-year-old man with osteoarthritis who presented
with hematemesis and melena stools. The patient took naproxen on a
daily basis.
DIFFERENTIAL DIAGNOSE
Nonulcer dyspepsia (NUD) or functional dyspepsia
Functional dyspepsia is a diagnosis of exclusion made in patients
with chronic persistent epigastric pain in whom a thorough
evaluation shows no organic disease. Patients may primarily
have epigastric pain, which is referred to as ulcerlike dyspepsia,
or they may have symptoms of postprandial bloating, which is
referred to as motility-like dyspepsia.
Crohn disease
Crohn ulceration can involve any part of the GI tract from the
buccal mucosa to the rectum. Isolated Crohn ulceration of the
stomach is rare, although it may cause duodenal or ileal
ulcerations.
Zollinger-Ellison syndrome
Zollinger-Ellison syndrome (ZES) is a rare disorder that can
cause gastric or duodenal ulcers (usually multiple) from
excessive acid secretion. Consider ZES if a patient has severe
peptic ulceration, kidney stones, watery diarrhea, or
malabsorption. ZES can also be associated with multiple
endocrine neoplasia type I, which occurs earlier than isolated
ZES. Patients with ZES usually have fasting serum gastrin levels
of more than 200 pg/mL and basal gastric acid hypersecretion of
more than 15 mEq/h. Proton pump inhibitor (PPI) therapy should
be discontinued at least 2 weeks before the gastrin level is
measured.

Differentials
Acute Coronary Syndrome
Aneurysm, Abdominal
Cholangitis
Cholecystitis
Cholecystitis and Biliary Colic in Emergency Medicine
Cholelithiasis
Diverticular Disease
Esophageal Perforation, Rupture and Tears
Esophagitis
Gastritis, Acute
Gastritis, Chronic
Gastroenteritis
Gastroesophageal Reflux Disease
Inflammatory Bowel Disease
Viral Hepatitis

TREATMENT
Treatment involves a combination of medications to
kill the H. pylori bacteria (if present), and reduce acid
levels in the stomach. This strategy allows your ulcer
to heal and reduces the chance it will come back.
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

An ulcer without an H. pylori infection, or one that
is caused by taking aspirin or NSAIDs 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)
If a peptic ulcer bleeds a lot, an EGD may be
needed to stop the bleeding. Surgery may be
needed if bleeding cannot be stopped with an
EGD, or if the ulcer has caused a perforation.

Alternative triple-therapy regimens
The alternative triple therapies, also administered for 14 days,
are as follows:
Omeprazole (Prilosec): 20 mg PO bid or Lansoprazole (Prevacid): 30
mg PO bid or Rabeprazole (Aciphex): 20 mg PO bid or Esomeprazole
(Nexium): 40 mg PO qd Plus Clarithromycin (Biaxin): 500 mg PO bid
and Metronidazole (Flagyl): 500 mg PO bid

Quadriple therapy
Quadriple therapies for H pylori infection are generally
reserved for patients in whom the standard course of
treatment has failed.
Quadriple treatment includes the following drugs, administered
for 14 days:
PPI, standard dose, or ranitidine 150 mg, PO bid
Bismuth 525 mg PO qid
Metronidazole 500 mg PO qid
Tetracycline 500 mg PO qid
Consider maintenance therapy with half of the standard doses
of H2-receptor antagonists at bedtime in patients with
recurrent, refractory, or complicated ulcers, particularly if cure
of H pylori has not been documented or if an H pylori
negative ulcer is present.


ULCERS THAT FAIL TO HEAL
Peptic ulcers that don't heal with treatment are called
refractory ulcers. There are many reasons why an ulcer
may fail to heal. These reasons may include:
Not taking medications according to directions.
The fact that some types of H. pylori are resistant to
antibiotics.
Regular use of tobacco.
Regular use of pain relievers that increase the risk of ulcers.
Less often, refractory ulcers may be a result of:
Extreme overproduction of stomach acid, such as occurs in
Zollinger-Ellison syndrome
An infection other than H. pylori
Stomach cancer
Other diseases that may cause ulcer-like sores in the stomach
and small intestine, such as Crohn's disease
Treatment for refractory ulcers generally involves
eliminating factors that may interfere with healing, along
with using different antibiotics.

PATIENT EDUCATION
Patients should be warned of known or potentially
injurious drugs and agents. Some examples are as
follows:
NSAIDs
Aspirin
Alcohol
Tobacco
Caffeine (eg, coffee, tea, colas)
Obesity has been shown to have an association with
peptic ulcer disease (PUD), and patients should be
counseled regarding benefits of weight loss.
Stress reduction counseling might be helpful in
individual cases but is not needed routinely.
Lifestyle and home remedies
Choose a healthy diet. Choose a healthy diet full
of fruits, vegetables and whole grains.
Consider switching pain relievers.
Control stress. Stress may worsen the signs and
symptoms of a peptic ulcer.
Don't smoke. stomach acid .
Limit or avoid alcohol. Excessive use of alcohol
can irritate and erode the mucous lining in stomach
and intestines, causing inflammation and bleeding.

PROGNOSIS
When the underlying cause is addressed, the
prognosis is excellent.
Most patients are treated successfully with eradication
of H pylori infection, avoidance of NSAIDs, and the
appropriate use of antisecretory therapy.
Eradication of H pylori infection changes the natural
history of the disease, with a decrease in the ulcer
recurrence rate from 60-90% to approximately 10-
20%.
With regard to NSAID-related ulcers, the incidence of
perforation is approximately 0.3% per patient year,
and the incidence of obstruction is approximately
0.1% per patient year.
Combining both duodenal ulcers and gastric ulcers,
the rate of any complication in all age groups
combined is approximately 1-2% per ulcer per year.
The mortality rate for PUD, which has decreased
modestly in the last few decades, is
approximately 1 death per 100,000 cases.
If one considers all patients with duodenal ulcers,
the mortality rate due to ulcer hemorrhage is
approximately 5%.
However, evidence from meta-analyses and other
studies has shown a decreased mortality rate
from bleeding peptic ulcers when intravenous
PPIs are used after successful endoscopic
therapy
Emergency operations for peptic ulcer perforation
carry a mortality risk of 6-30%.

Factors associated with higher mortality in this
setting include the following:
Shock at the time of admission
Renal insufficiency
Delaying the initiation of surgery for more than 12
hours after presentation
Concurrent medical illness (eg, cardiovascular
disease, diabetes mellitus
Age older than 70 years
Cirrhosis
Immunocompromised state
Location of ulcer (mortality associated with
perforated gastric ulcer is twice that associated with
perforated duodenal ulcer.)

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

PREVENTION
Avoid aspirin, ibuprofen, naproxen, and other
NSAIDs. Try acetaminophen instead.
The following lifestyle changes may help prevent
peptic ulcers:
Do not smoke or chew tobacco.
Limit alcohol to no more than two drinks per day.

GASTRITIS
Chronic Gastritis
Atrophic Gastritis
Erosive Gastritis
Variliform 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
The most common are:
Alcohol
Erosion (loss) of the protective layer of the stomach lining
Infection of the stomach with Helicobacter pylori bacteria
Medications such as aspirin or other nonsteroidal anti-
inflammatory drugs (NSAIDs)
Smoking
Less common causes are:
Autoimmune disorders (such as pernicious anemia)
Backflow of bile into the stomach (bile reflux)
Eating or drinking caustic or corrosive substances (such as
poisons)
Excess gastric acid secretion (such as from stress)
Viral infection, especially in people with a weak immune
system

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
Diagnosis

Upper endoscopy
Blood tests
Fecal occult blood test (stool test
Treatment
Mediacation
1.H2-blockers :
cimetidine (Tagamet), famotidine (Pepcid),niz
atidine (Axid), ranitidine (Zantac).
2.Proton pump inhibitors (PPIs) :
lansoprazole (Prevacid),omeprazole (Prilosec
, Losec).
3.Coating agents:
Sucralfate (Carafate), Misoprostol (Cytotec)
4.Antacids
5.Antibiotic
6.Antiemetic
Prevention
Avoid substances that trigger gastritis symptoms:
1. Cigarette smoking
2. Coffee and other beverages that contains caffein (cola,
tea)
3. Alcohol
4. Aspirin (use coated aspirin if you must take aspirin)
5. NSAIDs such as ibuprofen (Motrin, Advil) or naproxen
(Naprosyn)


Differential Diagnosis
Acute Coronary Syndrome
Gastroenteritis
Aneurysm, Abdominal
Hepatitis
Cholangitis
Inflammatory Bowel Disease
Cholecystitis and Biliary Colic
Mesenteric Ischemia
Cholelithiasis
Myocardial Infarction
Diverticular Disease
Pancreatitis
Esophageal Perforation, Rupture and Tears
Pulmonary Embolism
Esophagitis
Renal Calculi
Complications
Malignancy
Hemorrhage
Perforation
Obstruction

Prognosis
The prognosis is excellent. Most patients are cured
when the cause has been identified and treated
appropriately.

GERD
a condition in which the liquid content of the
stomach regurgitates (backs up or refluxes) into
the esophagus. The liquid can inflame and
damage the lining of the esophagus although
visible signs of inflammation occur in a minority of
patients.
Epidemiology
It rares in Asia-Africa but common seen in
europe countries
There is no epidemiology data in Indonesia,
but we can see 22,8 % esophagitis case in
RSCM from all gastrointestinal disease
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
etiology
hormonal
Anatomic
and physiology
environmental
genetic
neurogenic
Autosomal dominant (13q )
diet
smoking
Nervous X
Disorder of gastrin secretiong
Gastric emptying
Esophageal clearance
Anti reflux barrier
TLERS
Risk Factors
Dietary Habits
Eating large portions.
Eating certain foods,
including onions, chocolate,
peppermint, high-fat or spicy
foods, citrus fruits, garlic,
and tomatoes or tomato-
based products.
Drinking certain beverages,
including citrus juices,
alcohol, caffeinated drinks,
and carbonated drinks.
Eating before bedtime

Lifestyle Habits
Being overweight
Smoking
Wearing tight-fitting clothing or
belts
Lying down or bending over,
especially after eating
Stress
Medical Causes
Pregnancy
Bulging of part of the stomach into
the chest cavity, also called hiatal
hernia.
GERD.
Taking certain medications,
especially some antibiotics and
aspirin.


PATHOPYSIOLOGY
Esophagus and gaster are separated by a
high pressure zone as the result of Lower
Esophageal Sfingter contaraction.
Normally this pressure is defended, except
when swallowing, bleching and vomiting.
Reflux occurs when the gradient of
pressure between the LES and the
stomach is lost or under 3mmHg
/contraction of the LES is decrease.
The pathogenesis of reflux depend on the
balance of defensive and ofensive factors.
PATHOPHYSIOLOGY
DEVENSIVE FACTORS
1. Esophagus barrier
tonus of LES
2. Esophageal clearence
depend on gravitation,
peristaltic, saliva and
bicarbonate excretion
3. Epithelial resistence
Cell membrane
Differentiation of epithelial
tissue
Intracellular junction which is
bordering the diffusion of H
+

to esophageal tissue

OFENSIVE FACTORS
1. Gastric Secretion
2. Power of M. Sfingter
Pylorus
3. Delayed gatric emptying
Tonus of LES
Factors that decrease tonus of LES :
Hiatus Hernia
Occurs when the upper part of the stomach protrudes
up above the diaphragm into the chest -> the supporting
pressure from diaphragm to LES -> reflux
Length of LES
Short LES -> tonus of LES ->reflux
Drugs
anticholinergic, beta-adrenergic, opioid -> tonus of LES
->reflux
Hormonal Factors
Gastrin -> HCl secretion -> insidens of reflux is
increase
Pregnancy -> progrestran secretion -> tonus of LES -
>reflux

Mechanisme Reflux in Normal Tonus of LES
Transient Lower Esophageal Sfingter
Relaxation
Spontanious LES relaxation ( 5s) without
early swalowing process -> reflux stomatch
content

Mechanisme is idiophatic, possibility :
- Delayed gastric emptying
- Gastric dilatation
- Gastric obstruction
- Neuroreflex disorder
Pathophyisiology
Extraesophageal Manifestations of
GERD:
Pulmonary
Asthma
Aspiration
pneumonia
Chronic bronchitis
Pulmonary fibrosis

Other
Chest pain
Dental erosion

ENT
Hoarseness
Laryngitis
Pharyngitis
Chronic cough
Globus sensation
Dysphonia
Sinusitis
Subglottic stenosis
Laryngeal cancer

Barium Swallow
Useful first diagnostic test for patients
with dysphagia
Stricture (location, length)
Mass (location, length)
Birds beak
Hiatal hernia (size, type)
Limitations
Detailed mucosal exam for erosive
esophagitis, Barretts esophagus
Most useful for detecting peptic
strictures


Endoscopy
Indications for endoscopy
Alarm symptoms
Empiric therapy failure
Preoperative evaluation
Detection of Barretts esophagus
SPECTRUM OF ENDOSCOPIC FINDINGS
WITH GERD
Normal esophagus Grade 3 esophagitis
Grade 4 esophagitis Barretts esophagus
Ambulatory 24 hr. pH Monitoring
Physiologic study
Quantify reflux in
proximal/distal
esophagus
% time pH < 4
DeMeester score
Symptom
correlation

Diognostic for Infant

GERD Treatment
Lifestyle changes
Infant: alterations in formula compositions
(thickening formula), sleep positioning
Adolescents: 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 Lifestyle Changes
Position therapy:
Less GER in prone than in supine. Similar
reflux in left, right, & supine positions
Prone is superior to semi supine positioning in
infant seat
However, supine has < risk of sudden
infant death syndrome, thus,
recommended positions are:
Prone when infant is awake, supine positioning
during sleep
Older children & Adult benefits from
head elevation, less GER in LLD than in
RLD

Treatment Pharmacotherapy

Step up & Step down Therapy
Approach to acid reducing therapy:
Step up:
Begin: H2RA at standard dosage, following with a
PPI at standard dosage and then a PPI at higher
dosage if necessary to achieve improvement
Step down
Begin: PPI at higher dosage to achieve
improvement, following with a PPI at standard
dosage and then an H2RA to maintain improvement
Adults step down > cost effective &
recommended, but there are no published
studies in children
Drugs demonstrated to be effective in gastroesophageal reflux disease
(North American Society of Pediatric Gastroenterology and Nutrition)
Treatment Surgery
Surgery, usually fundoplication:
Effective th for intractable GERD particularly those
with refractory esophagitis or strictures and those at
risk for significant morbidity from chronic pulmonary
disease.
It may be combined with a gastrostomy for feeding
or venting
Long term studies suggest fundoplication frequently
become incompentent in children & adults (due
uses of PPI for long term pharmacotherapy)
Some of the risks of fundoplication include a wrap
that is "too tight" (producing dysphagia or gas-bloat)
or "too loose (and thus incompetent)
Tight (360, Nissen), loose (< 360, Thal) wrap

Therapy
Stage 1 Heartburn < 2-3x/week Lifestyle changes, diet,
position, weight-losing.
Antacid, receptor H2
antagonis
Stage 2 Heartburn with esofagitis,
>2-3x/week
PPI (omeprazole,
esomeprazole,
rabeprazole,
lansoprazole)
Stage 3 chronic, continue signs and
symptoms, relaps,
esophagus complication
PPI (omeprazole,
esomeprazole,
rabeprazole,
lansoprazole)
Treatment
Treatment
Life style
modification
Elevation of the upper body at night generally is recommended for all patients
with GERD
GERD Diet
* These foods should be avoided and include:
Chocolate, peppermint, alcohol & caffeinated drinks
* Fatty foods (which should be decreased) and smoking (which should be
stopped) also reduce the pressure in the sphincter and promote reflux
* Chewing gum stimulates the production of more bicarbonate-containing saliva
and increases the rate of swallowing.
Antacids
Antacids neutralize the acid in the stomach so that there is no acid to reflux
they do so for only a short period of time
The best way to take antacids, therefore, is approximately one hour after meals
or just before the symptoms of reflux begin after a meal. Since the food from
meals slows the emptying from the stomach, an antacid taken after a meal
stays in the stomach longer and is effective longer
Histamin
Antagonist
The first medication developed for more effective and convenient treatment of
acid-related diseases, including GERD, was a histamine antagonist, specifically
cimetidine (Tagamet)
Histamine is an important chemical because it stimulates acid production by the
stomach
Four different H2 antagonists are available by prescription, including cimetidine
(Tagamet), ranitidine (Zantac), nizatidine (Axid), and famotidine, (Pepcid)

Treatment
Protein Pump
Inhibitor
The second type of drug developed specifically for acid-related diseases,
such as GERD, was a proton pump inhibitor (PPI), specifically, omeprazole
(Prilosec)
The advantage of a PPI over an H2 antagonist is that the PPI shuts off acid
production more completely and for a longer period of time
Five different PPIs are approved for the treatment of GERD, including
omeprazole (Prilosec), lansoprazole (Prevacid), rabeprazole (Aciphex),
pantoprazole (Protonix), and esomeprazole (Nexium). A fifth PPI product
consists of a combination of omeprazole and sodium bicarbonate (Zegerid).
PPIs (except for Zegarid) are best taken an hour before meals
Pro Motility Drug
Pro-motility drugs work by stimulating the muscles of the gastrointestinal
tract, including the esophagus, stomach, small intestine, and/or colon. One
pro-motility drug, metoclopramide (Reglan)
Pro-motility drugs increase the pressure in the lower esophageal sphincter
and strengthen the contractions (peristalsis) of the esophagus
Foam Barriers
Foam barriers are tablets that are composed of an antacid and a foaming
agent.
There is only one foam barrier, which is a combination of aluminum
hydroxide gel, magnesium trisilicate, and alginate (Gaviscon).
Surgery The surgical procedure that is done to prevent reflux is
technically known as fundoplication and is called reflux
surgery or anti-reflux surgery
Endoscopy
It is not clear how effective they are, especially long-term. Because the
effectiveness and the full extent of potential complications of endoscopic
techniques are not clear, it is felt generally that endoscopic treatment
should only be done as part of experimental trials.
http://www.gerd.com/intro/noframe/grossovw.htm
Esophageal
clearance:
Cisapride
Esophageal mucosal
resistance: Alginic
acid, Sucralfate
Gastric emptying:
Metoclopramide
Cisapride
LES pressure:
MetoclopramideCi
sapride
Gastric acid:
Antacids
H2RAs PPIs
Breastfeeding
Breastfeeding is definitely best for a baby with reflux
because it is more hypoallergenic than formula and is
digested twice as fast as formula.
Feeding Time
Smaller more frequent meals through out the day work much
better than larger, less frequent meals.
Avoid feeding baby right before bedtime

Complications
Barretts esophagus (a change in the lining of
the esophagus that can increase the risk of
cancer)
Bronchospasm (irritation and resulting spasm
of airways due to acid)
Chronic pulmonary disease
Esophageal ulcer
Hoarseness
Inflammation of the esophagus
Stricture (a narrowing of the esophagus due
to scarring from the inflammation)
Prognosis
The majority of people respond to nonsurgical
measures, with lifestyle changes and
medications.
However, many patients need to continue to take
drugs to control their symptoms.

Prevention
Maintain a healthy body weight.
Avoid large meals and eating within 3 hours of
bedtime.
Limit fatty or greasy foods, chocolate, caffeine, and
other irritating foods.
Avoid alcohol.
Stop smoking.
Avoid working out, bending, or stooping on a full
stomach

Prevention
DD
Bowel Obstruction:
Blockage in the bowel of the digestive tract.
Cyclic vomiting syndrome:
A rare disorder involving repeated cyclic episodes
of vomiting which occur for no obvious reason.
Pyloric stenosis:
Narrowed opening between stomach and intestines
Hiatus Hernia
Which causes LES doesnt work as it supposed to
be


REFERENCES
http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0
001255/
http://emedicine.medscape.com/article/181753-
differential