Pharmacy Clinic
Peptic Ulcer and Heart Burn


CEASES OF ULCER:

The stomach produces hydrochloric acid and enzymes to help digest the food you eat. Normally, the stomach and
duodenum are protected from damage by these substances. In the stomach, a layer of mucous covers the lining to
protect it from the acid.

In the duodenum, fluid from the pancreas neutralizes the acid before any damage occurs. An ulcer forms either
because of:

*Too much acid
      
        or         

*some weakness in these normal protective mechanisms.

Many peoples with gastric ulcer produce normal or less than normal amount of acid. For this reason, we know that
acid is not the only factor involved in the formation of ulcers.

Factors related to the formation of ulcer:

Many factors that contribute in the formation of an ulcer, may be acquired during life.

In the past they believed that no acid no ulcer, but now it is believed that ulcer results from a complex interplay of acid
and chronic inflammation induced by bacterial infection even though the exact mechanism has not been elucidated,
other causes are the NSAID's, tumors like Zollinger Ellison syndrome, other causes with a minor effect like smoking,
emotional stress ulcer (stress related to work, family problems or any thing that cause such emotional things.

The reason for this type (emotional) of ulcer is believed that the mucous secretion depends on the blood flow in the
mucosal cells, during anger the brain send signals that close stomach blood vessels, mucous secretion was diminishes
and the exposure to hard conditions make the stomach susceptible to ulcer but this not ready to cause severe ulcer,
maybe heartburn).

First                Helicobacter Pylori

Pathophysiology of Helicobacter pylori

Helicobacter pylori (called Campylobacter pylori) is a curved or S-shaped bacterium found in close contact with the
mucosa in the antrum of the stomach, often in grooves between cells under a stable layer of mucus that shields the
organisms from gastric acid. H. Pylori is almost always present when inflammation is present, and they are rare when
inflammation is absent.
Infection of the mucosa damages epithelial cells and reduces mucus viscosity. With the mucous layer impaired, gastric
acid and pepsin cause epithelial erosion and ulceration.
Thus gastric acid, while not directly responsible for peptic ulceration, plays a contributory role.
By reducing acid secretion, the H2- antagonists are able to heal 80-90% of peptic ulcers after one year of therapy,
but relapse rates are high when the drug is withdrawn (up to 85% the first year and up to 100% the second year). By
contrast, antibiotic therapy has an excellent success rate.

Once H. pylori is identified and eradicated, gastritis and peptic ulcers usually heal and stay healed. Left untreated, the
infection may persist for life, and so may the ulcer.

The Epidemiology of Helicobacter pylori Infection

Helicobacter pylori causes what is probably the most common human infection in the world.
Medical researchers in dozens of countries on almost every continent have shown that the bacterium infects the
gastric mucous layer of almost all patients with duodenal ulcer disease, most patients with gastric ulcer disease, and
almost all patients with histologic antral gastritis.

Epidemiologic studies have shown that H. pylori infection is more common in individuals with low income than in those
with high income; it is more common in blacks and Hispanics  than in non-Hispanic whites; and it is more common
among the elderly. Approximately 50% of North Americans over age 50 are infected with H. pylori, while some two
thirds of Britons  over age 70 are similarly infected. In some developing countries, H. pylori infects almost all adults.
How is H.Pylori acquired? Prospective family studies have indicated that the bacterium is contagious. In some areas, it
can be acquired through drinking contaminated water. In Peru, where H. pylori infection is common in infants,
investigators turned up an association between drinking the water from municipal water  supplies as opposed to using
water from wells or cisterns

In most cases, when H. pylori infection is cleared, ulcer disease is cured and the risk of relapse is markedly reduced.
Researchers don't yet know whether ulcers recur if the patient is reinfected, although it does appear that reinfection
rates may be low. Eradication of infection in family members may not be necessary to prevent reinfection or reduce its
rate in index cases.

When ulcers are refractory to antibiotic therapy, the patient is usually on long-term therapy with a nonsteroidal
antiinflammatory drug (NSAID) or has a disorder involving pathologic acid hypersecretion (such as Zollinger-Ellison
syndrome).

Generally, however, most ulcers are curable. This news has come as quite a relief to ulcer patients, who have been told
for years to eat a restricted diet, stop smoking, and avoid stress. When they suffer a relapse, they are told they still
aren't handling stress or complying with diet. They are happy to find out they are infected, not incompetent.

Etiology

H.Pylori infection weakens the lining and may allow an ulcer to form. These ulcers may heal with the usual antiulcer
drugs, but often recur when treatment is stopped.

Antibiotics may cure the infection and allow the ulcer to heal. In addition to helping the ulcer heal, eradication of this
infection may eliminate the tendency to develop recurrent ulcers.

In 1982 Biopsies obtained from mucosal stomach lining of patients suffering from chronic gastritis and more severe
conditions, peptic ulcer disease, H.Pylori was cultured from these biopsies.

About 95% of persons with gastric ulcers and 100% of persons with chronic gastritis have this bacterium within the
stomach .

This bacterium is known to bind to the O blood-group structure present on gastric epithelial cells (a person who is O-
positive is about twice as likely to develop stomach ulcers relative to O-negative persons).
H. pylori can convert the substance called urea, to carbon dioxide (gas) and another substance called ammonia. Urea
is a normal chemical product of the biochemical pathway in our body used to eliminate many nitrogen-containing
compounds from our system (excreted in the urine).

H. pylori products are very active forms of the urease enzyme. The ammonia produced from urease action on urea,
neutralizes the acid in the area where the bacteria are growing, and allows the bacteria to become established and to
grow (an infection) within the epithelial tissue. The organism produces substances which cause tissue damage, and,
the body's immune  defense system through fighting the infection, causes further local tissue damage.
After a time, the damaged tissue no longer can secrete mucous properly, which allows the acid and enzymes to also
begin to attack the tissue. The mucosal layer will damaged and the resultant from damaging the tissue is an ulcer.
It is thought that H.Pylori survive in highly acidic environment by hydrolyzing urea to make ammonia. Which
neutralizes stomach acid in the immediate vicinity of the bacteria. They also suppress acid production by damaging the
stomach cells. Then, when the patient’s immune response succeeds in suppressing the bacteria, acid secretion returns
to normal and the acid digests the damaged cells, leading to chronic gastritis and ulcers.
It still is unclear what exact role H.Pylori plays in the pathogenesis of peptic ulcer disease and whom it will affect
adversely. However, eradication of the organism in patients with recurrent ulcers does seem to change the natural
history of the disease.

Second        NSAID's

Aspirin, ibuprofen, and many antiarthritis drugs (Non Steroidal anti Inflammatory Drugs or NSAID's) weakens the
lining of the stomach and can cause ulcers. These drugs slow the production of prostaglandins.

The most common site of action on NSAID's associated with the ulcer is the antral portion of the stomach or the body
of the stomach.

NSAID's produce gastric damages by two different ways:

1)        Direct irritant effect
2)        Systemic effect

So both rectal and intravenous administration of these drugs cause an ulcer despite the absence of the direct mucosal
contact.

The more water soluble analgesics are more likely to produce direct irritant effect ex. Aspirin. Enteric coated tablets
also induce gastric irritation but to a lesser extent, but here do this by systemic effect.

The exact mechanism by which NSAID's induce the systemic effect of gastric irritation is still unclear, but they thought
that the inhibition of prostaglandin is the most expected cause for the gastric ulceration because prostaglandin in the
mucus layers act as a defensive product which increase the release of mucus and bicarbonate which act as a
neutralizer for the high acidity in the stomach.

Not only the inhibition of prostaglandin is the cause of ulcer, NSAID's also interfere with the cellular and mitochondrial
metabolism and the immune and inflammatory reaction of the mucosa.

The use of NSAID's with patients suffered from a history of peptic ulcer may increase the risk of gastric irritation.
Cytotec is a synthetic prostaglandin which can prevent ulcers from occurring as a result of taking NSAID's. The most
common side effects of Cytotec are nausea and diarrhea.

Stress Ulcer
This type of ulcer is extremely different than any other ulcer, it needs no history of ulceration to happens, it related to
critical; ill patients, so 75 100% of critically ill patients have gastric lesions.

The cause of stress ulcer depends on the balance between the aggressive forces and defensive forces. When the
imbalance occur and the defensive forces impaired the aggressive forces like acid and pepsin act to produce a
superficial lesions, the removal of these aggressive forces will recur the lesions in the GI Tract.

The presence of acid is the causative agent in stress ulcer not the quantity of acid release.

In critically ill patients the flow of blood to the digestive system is decreased causing:

1) Decreased nutrient and oxygen delivery
2) Inability of the mucosa to remove or neutralize acid..
3) Decrease bicarbonate production in the gastric epithelium
4) Decreased in the cellular turnover of the gastric mucosa.


Treatment options

what is heartburn?

What is ulcer?