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Yusnadi yonatan

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Anatomy
Histologi GIT In the oesophagus, the
mucosa is formed by a
stratified squamous
epithelium (non-
keratinised)
Oesophageal glands are
located in the submucosa.
These submucosal glands
produce a mucous secretion,
which lubricates the
epithelium and aids the
passage of food. The mucous
glands in the part of the
oesophagus closest to the
stomach protect the
oesophageal mucosa from
acidic reflux from the
stomach.
The adventitia consists only
of a layer of loose connective
tissue. Only the lowest part of
the oesophagus (approx. the
lowest 2 cm) enters the
peritoneal cavity.
Histologi
Chief cells (or
zymogenic cells)
They produce
pepsinogen, which is
a precursor of the
proteolytic enzyme
pepsin.

Parietal cells (or


oxyntic cells)
Parietal cells secrete
the hydrochloric acid
of the gastric juice
Histology of Ileum
VOMITING
Complication
Metabolic disorder
Nutritional disorder
Mallory Weiss tear
Esophagitis
Aspiration
Shock
SYNDROME OF DYSPEPSIA
persistent or recurrent upper
abdominal pain or discomfort
characterized by postprandial
fullness, early satiety, nausea, and
bloating.
SYNDROME OF DYSPEPSIA
Epidemiology: Each year 10-20% of US
population seeks medical attention.
NUD 2-3 x peptic ulcer disease.
Etiology & Pathogenesis:
Imbalance of the aggravating factors
and defensive factors. The aggravating
factor increased and the defensive
factors decrease will cause functional
and organic /ulcer dyspepsia.
AGGRAVATING FACTORS OF
SYNDROME DYSPEPSIA:
Gastric acid
Pepsin
Helicobacter pylori infection
Gastric motor activity: 25-50% patients exhibit postprandial
antral hypomotility or delayed gastric emptying
Psychological factors: anxiety and depression
Diet: foods: spicy/hot, sour, vinnegar, drinks: coffee,
smoking/tobacco, alcohol
Drugs: non-steroidal anti-inflammatory drugs(nsaid), traditional
pain killer drugs, steroids, antibiotics(erythromycin, ampicillin),
iron, potassium, digoxin, theophylline.
Metabolic diseases: diabetes mellitus, hypothoroidism
Hypopotassemia.
Free radicals
DEFENSIVE FACTORS OF SYNDROME
DYSPEPSIA:
Prostaglandin
Mucus
Mucosal blood flow
Surfactant
Bicarbonat
Heat shock protein
Epitel/preepithelial factors
etc
CLINICAL FEATURES IN SYNDROME
DYSPEPSIA
Non Ulcer Disease:
Ulcer like: dominant epigastric pain, relieved by
antacids or food
Dysmotility like: epigastric discomfort
aggravated by food or associated with early
satiety, fullness, nausea, retching, vomiting, or
bloating.
Nonspecific: symptoms does not fit the other
categories
Reflux like: heartburn and regurgitation
Ulcer: the same with NUD
PHYSICAL EXAMINATION IN
SYNDROME DYSPEPSIA
not specific
epigastric tenderness some times
abdominal mass if advanced gastric
carcinoma
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).
This action can irritate the esophagus,
causing heartburn and other symptoms.
Gastroesophageal reflux is a common
condition that often occurs without
symptoms after meals.
Epidemiology
Infant reflux becomes evident: 1st few mo
of life, peaks at ~ 4 mo, resolves in most
by 12 mo and nearly all by 24 mo
Common: America & Europe; relatively low
incidence in Asia Africa
GERD likely has genetic predispositions
Family clustering of GERD symptoms,
endoscopic esophagitis, hiatal hernia,
Barretts esophagus, & adenocarcinoma
has been identified
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
Pathophysiology
Transient LES Relaxation (TLESR): primary
mechanism allowing reflux to occur
TLESR = independent of swallowing, reducing
LES pressure to 0-2mmHg, last >10sec; appear
by 26wk gestation
Gastric distention (postprandially, or due to
abnormal gastric emptying, or air swallowing)
main stimulus
GERD is caused whether by increased
frequency of TLESR or greater incidence of
reflux during TLESR is still debated
Risk factors: positions, factors that influencing
gastric pressure-volume dynamics (eg:
increased movement, straining, obesity, large
volume or hyperosmolar meals, increased
respiratory effort [cough, wheeze])
GERD Clinical
Manifestations
Infantile reflux
More often w/ regurgitation (especially postprandially), signs of
esophagitis (irritability, arching, choking, gagging, feeding
aversion), & resulting failure to thrive
Symptoms resolve spontaneously in the majority by 12-24 mo
May manifest as obs apnea, or as stridor (in which reflux
complicates primary airway disease*)
Older children
May have regurgitation preschool years; complaints of abd &
chest pain later childhood & adolescence
Occasional children present w/ neck contortions (arching,
turning of head) Sandifer Syndrome
Airway manifestations in older children frequently related to
asthma, otolaryngologic disease (eg: laryngitis, sinusitis)
GERD Clinical
Manifestations
Otitis media, sinusitis, lymphoid
hyperplasia, hoarseness, vocal cord
nodules, & laryngeal edema have
all been associated w/ GERD
Other symptoms:
Belching, Cough or wheezing, Difficulty
swallowing, Heartburn, Hoarseness,
Nausea and vomiting, Regurgitation of
food, Sore Throat, Vomiting Blood
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: H RA at standard dosage, following with a PPI at
2

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
H RA to maintain improvement
2

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
Complications
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)
Hold the baby upright for a Propping a baby up after
time after feeding to help feeding helps keep fluid from
prevent spitting up. traveling up from the
stomach.

30 degree

The Acid Reflux Wedge Pillow For Baby


Posisition of feeding

Prevention
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.
Gastritis
Definition: inflammation of the
gastric mucosa
Acute Gastritis
Chronic Gastritis
Acute Gastritis
Acute gastritis is a term covering a broad
spectrum of entities that induce
inflammatory changes in the gastric
mucosa. Acute gastritis can be broken
down into 2 categories:
erosive (e.g, superficial erosions, deep
erosions, hemorrhagic erosions)
non-erosive (generally caused by
Helicobacter pylori)
Symptoms include nausea, vomiting, loss
of appetite, belching, and bloating.
Occasionally, acute abdominal pain can be
a presenting symptom.
One or more of the following influences
are thought to be operative in these varied
settings:
Disruption of the adherent mucous layer
Stimulation of acid secretion with hydrogen ion
back diffusion into the superficial epithelium
Decreased production of bicarbonate buffer by
superficial epithelial cells
Reduced mucosal blood flow
Direct damage to the epithelium
Risk Factors
Acute gastritis is frequently associated
with:
Heavy use NSAID, particularly aspirin
Excessive alcohol consumption
Heavy smoking
Treatment with cancer chemotherapeutic drugs
Systemic infections (eg. Salmonellosis)
Severe stress (eg. Trauma, burns, surgery)
Ischemia and shock
Suicide attempts with acids and alkali
Mechanical trauma (eg. Nasogastric intubation)
Reflux of bilious material after distal
gastrectomy
Sign and Symptoms
Acute gastritis may be entirely
asymptomatic
Epigastric pain
Nausea
Vomiting
Hematemesis
Melena
Potentially fatal blood loss
25% of persons who take daily
aspirin for rheumatoid arthritis
develop acute gastritis at some time
in their course, many with occult or
overt bleeding
The risk of gastric bleeding from
NSAID induced gastritis is dose
related, thus increasing the likelihood
of this complication in persons
requiring longterm use of such drugs
Chronic Gastritis
Definition: the presence of chronic
inflammatory changes in the mucosa
leading eventually to mucosal atrophy and
epithelial metaplasia
Most individuals with the infection also
have the associated gastritis but are
asymptomatic
Epidemiology: american adults older than
age 50 show prevalence rates approaching
50%. In areas where the infection is
endemic, it seems to be acquired in
childhood and persists for decades
Pathophisiology
Most important etiologic association is
chronic infection by the bacillus H. pylori
Gastritis develops as a result of the
combined influence of bacterial enzymes
and toxins and release of noxious
chemicals by the recruited neutrophils
Characterized by mononuclear cell
infiltration in the lamina propia with
intestinal metaplasia and frequently
proliferation of lymphoid tissue
After initial exposure to H. pylori,
gastritis may develop in 2 patterns:
An antral-type with high acid production
and higher risk for the development of
duodenal ulcer
A pangastritis with multifocal mucosal
atrophy, with low acid secretion and
increased risk for adenocarcinoma
Sign and Symptoms
Usually causes few or no symptoms
Upper abdominal discomfort
Nausea
Vomiting
Most important is the relationship of
chronic gastritis to the development
of peptic ulcer and gastric carcinoma
Most individuals with a peptic ulcers,
whether duodenal or gastric, have H.
pylori infection
Duodenal Ulcer
A duodenal ulcer is a raw area in the
lining in the upper part of the small
intestine (duodenum), where it
connects to the stomach.
Etiology
Infection with Helicobacter pylori
More than a quarter of people in the UK become infected
with H. pylori at some stage in their life. Once you are
infected, unless treated, the infection usually stays for the
rest of your life. In many people it causes no problems and
a number of these bacteria just live harmlessly in the lining
of the stomach and duodenum. However, in some people
this bacterium causes an inflammation in the lining of the
stomach or duodenum. This causes the defence mucus
barrier to be disrupted (and in some cases the amount of
acid to be increased) which allows the acid to cause
inflammation and ulcers.
Anti-inflammatory drugs - including aspirin
However, these drugs sometimes affect the mucus barrier
of the duodenum and allow acid to cause an ulcer. About 1
in 20 duodenal ulcers are caused by anti-inflammatory
drugs.
Other causes and factors
Other causes are rare. For example, the Zollinger-Ellison
syndrome. In this rare condition, much more acid than
usual is made by the stomach. Other factors such as
Symptoms
Pain in the upper abdomen just below the
sternum (breastbone) is the common
symptom. It usually comes and goes. It
may occur most before meals, or when
you are hungry. It may be eased if you eat
food, or take antacid tablets. The pain may
wake you from sleep.
Other symptoms which may occur
include: bloating, retching, and feeling
sick. You may feel particularly 'full' after a
meal. Sometimes food makes the pain
worse.
Test
Endoscopy is the test that can confirm a
duodenal ulcer. In this test a doctor or nurse looks
inside your stomach and duodenum by passing a
thin, flexible telescope down your oesophagus.
They can see any inflammation or ulcers.
A test to detect the H. pylori bacterium is
usually done if you have a duodenal ulcer. If H.
pylori is found then it is likely to be the cause of
the ulcer. Briefly, it can be detected in a sample
of faeces, or in a 'breath test', or from a blood
test, or from a biopsy sample taken during an
endoscopy.
Treatment
Acid suppressing medication
A 4-8 week course of a drug that greatly reduces the amount of
acid that your stomach makes is usually advised. The most
commonly used drug is a proton pump inhibitor (PPI). These
are a class (group) of drugs that work on the cells that line the
stomach, reducing the production of acid. They include:
esomeprazole, lansoprazole, omeprazole, pantoprazole and
rabeprazole, and come in various brand names. Sometimes a drug
from another class of drugs called H2 blockers is used. H2
blockers work in a different way on the cells that line the stomach,
reducing the production of acid. They include: cimetidine,
famotidine, nizatidine and ranitidine, and come in various brand
names. As the amount of acid is greatly reduced, the ulcer usually
heals. However, this is not the end of the story ...
If your ulcer was caused by H. pylori
Nearly all duodenal ulcers are caused by infection with H. pylori.
Therefore, a main part of the treatment is to clear this infection. If
this infection is not cleared, the ulcer is likely to return once you
stop taking acid-suppressing medication. Two antibiotics are
needed. In addition, you need to take an acid-suppressing drug to
reduce the acid in the stomach. This is needed to allow the
antibiotics to work well. You need to take this 'combination therapy'
(sometimes called 'triple therapy') for a week.
After treatment, a test to check that H. Pylori has gone may be advised. If
it is done it needs to be done at least four weeks after the course of
combination therapy has finished. In most cases, the test is 'negative'
meaning that the infection has gone. If it has not gone, then a repeat
course of combination therapy with a different set of antibiotics may be
advised. Some doctors say that for people with a duodenal ulcer, this
'confirmation' test is not necessary if symptoms have gone. The fact that
symptoms have gone usually indicates that the ulcer and the cause (H.
pylori) have gone. But, some doctors say it is needed to play safe. Your
own doctor will advise if you should have it. (Note: a test to confirm that H
pylori has gone is usually always recommended if you have a stomach
ulcer.)
If your ulcer was caused by an anti-inflammatory drug
If possible, you should stop the anti-inflammatory drug. This allows the
ulcer to heal. You will also normally be prescribed an acid-suppressing drug
for several weeks (as mentioned above). This stops the stomach from
making acid and allows the ulcer to heal.
Surgery
In the past, surgery was commonly needed to treat a
duodenal ulcer. This was before it was discovered that H.
pylori was the cause of most duodenal ulcers, and before
modern acid-suppressing drugs became available. Surgery
is now usually only needed if a complication of a duodenal
ulcer develops such as severe bleeding or a perforation.
Complications
Bleeding ulcer. This can range from a
'trickle' to a life-threatening bleed.
Perforation. This is where the ulcer
goes right through ('perforates') the
wall of the duodenum. Food and acid
in the duodenum then leak into the
abdominal cavity. This usually causes
severe pain and is a medical
emergency.
Peptic Ulcer
Definition
A peptic ulcer is erosion in the lining of the stomach
or the first part of the small intestine, an area called
the duodenum.

PU includes
Duodenal ulcer. (commonest)
Gastric ulcer.
Common causes of PU
Infection with H.pylori.

NSAID and the usual suspects


(Alcohol ,smoking,
stress)

Imbalance between the


aggressive and protective
mechanisms.

Acid hypersecretion due to


increase number of parital cells
or as seen in (Zollinger-Ellison
syndrome).
Clinical Features (PU)

Small ulcers may not cause any symptoms. Large


ulcers can cause serious bleeding.
Abdominal pain is a common symptom but it doesn't
always occur.
M > F ,20-50 yrs.
Epigastric pain during fasting (hunger pain), relieved
by food and Antacids.
Back pain if ulcer is penetrating posteriorly.
Hematemesis from ulcer penetrating GD artery
posteriorly.
Can lead to peritonitis if ulcer occurs anteriorly.
Other possible symptoms include:
* Belching
* Bloody or dark tarry stools
* Chest pain
* Fatigue
* Heartburn
* Indigestion
* Nausea
* Vomiting, possibly bloody
* Weight loss
Exams and Tests
To diagnose an ulcer, your doctor will order one of the
following tests:
* Esophagogastroduodenoscopy (EGD)
* Upper GI is a series of x-rays taken after you drink a
thick substance called barium.
Your doctor may also order these tests:
* Hemoglobin blood test to check for anemia
* Stool guaiac to test for blood in your stool
Treatment
Treatment involves a combination of medications to kill
the H. pylori bacteria (if present), reduce acid levels,
and protect the GI tract. This strategy allows your
ulcer to heal and reduces the chance it will come back.
Medications may include one or more of the following:
* Acid blockers (such as cimetidine, ranitidine, or
famotidine)
* Antibiotics to kill H. pylori
* Bismuth to help protect the lining and kill the
bacteria
* Medications that protect the tissue lining (such as
sucralfate)
* Proton pump inhibitors such as omeprazole
(Prilosec), lansoprazole (Prevacid), or esomeprazole
(Nexium)
If you have an ulcer without an H. pylori infection, your
doctor will likely prescribe a proton pump inhibitor for
8 weeks. You may also be prescribed this type of
medicine if you must continue taking aspirin or NSAIDs
for other health conditions.
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

Prevention
Lifestyle changes may help prevent peptic
ulcers:
Tips include:
* Avoid aspirin, ibuprofen, naproxen, and other
NSAIDs. Try acetaminophen instead. If you
must take such medicines, talk to your doctor
first.
* Don't smoke or chew tobacco.
* Limit alcohol to no more than two drinks per
day.
Gastric Ulcer

Type Type
I IISame
M>F 3:1 , 50+ yrs.
Epigastric pain induced by as PU
eating.
Weight loss.
Nausea and vomiting.
Anaemia from chronic
blood loss.
Drug 1 Drug 2 Drug 3 Drug 4
PPI Clarithomycin Amoxcycyline
e

PPI Clarithomycin Metronidazole


e
PPI Tetracycline Metronidazole Subsalicylate
Drugs Example / Subcitral
Antacide Mylanta, maalox, tums,
gaviscon
Antagonist H2 Receptor Cimetidine, ranitidine,
famotidine, nizatidinie
PPI Omeprazole,
lansoprazole,
rabeprazole,
pantoprazole,
esomeprazole
Protective Mucous sucralfate
Sucralfate drug
Prostaglandin Analog misoprostol
Bismuth Drugs Bismuth, subsalicylate

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