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405090079
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.
30 degree
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.
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