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POST TIME: 28 November, 2016 00:00 00 AM
Peptic ulcer diseases

Peptic ulcer diseases

A peptic ulcer is a round or oval sore where the lining of the stomach or duodenum has been eaten away by stomach acid and digestive juices. We can also say that the term peptic ulcer, also called peptic ulcer disease, refers to an ulcer or a break in the gastric (stomach) or duodenal (beginning of the small intestine) mucosa that arises when the normal mucosal defensive factors are impaired or are overwhelmed by aggressive luminal factors such as acid an pepsin.

Ulcers develop when the lining of the stomach or duodenum is chronically inflamed or exposed to irritants, such as excess stomach acid and digestive enzymes, such as pepsin. Almost everyone produces stomach acid but only 1 of 10 people develops ulcers at some point during his or her lifetime.

Ulcers penetrate into the lining of the stomach or duodenum. Gastritis may develop into ulcers. The names given to specific ulcers identify their anatomic locations of the circumstances under which they develop. Duodenal ulcers the most common type of peptic ulcer, occur in the duodenum, the first few inches of small intestine just below the stomach.

Gastric ulcers, which are less common, usually occur along the upper curve of the stomach. Marginal ulcer can develop when part of the stomach has been removed surgically, at the point where the remaining stomach has been reconnected to the intestine. As with acute stress gastritis, stress ulcers can occur under the stress of severe illness, skin burns or trauma. Stress ulcers occur in the stomach and the duodenum.

Causes
Ulcers develop when the lining of the stomach or duodenum is chronically inflamed or exposed to irritants, such as excess stomach acid and digestive enzymes, such as pepsin. Almost everyone produces stomach acid but only 1 of 10 people develops ulcers at some point during his or her lifetime.

Different people generate different amounts of stomach acid and a person’s pattern of acid secretion tends to persist throughout life. People who normally secrete more acid have a greater tendency to develop peptic ulcers. However, other factors besides acid secretion are involved, because most people who are high secretors never develop ulcers and some people who are low secretors do develop them.

By far, the other two most common causes of peptic ulcer are infection with helocobacter pylori bacteria and use of certain drugs. Many drugs including aspirin, other non-steroidal anti-inflamatory drugs (NSAIDs) and corticosteroid, irritate the stomach lining and can cause ulcer.

However, the does not happen with all the people taking NSAIDs and or corticosteroids. Regardless, some experts suggest that people at high risk of developing peptic ulcers should use a new type of NSAID called a coxib. It is thought that coxibs are less likely to irritate the stomach.

Other contributory factors include:
a. Genetic factor :
1) Blood group – patient with duodenal ulcer largely belong to blood group “O”.
2) Antigen HLAB5 patient having duodenal ulcer have an increased incidence of HLAB5 antigen.
3) PGI- duodenal ulcer patients usually contain an increased serum pepsinogen level (PGI).
b. Reduced mucosal resistance:
1) Back diffusion of H+
2) Reflux of bile and intestinal secretion to stomach
3) Miscellaneous such as cigarette smoking – inhibits the secretion of pancreatic bicarbonate by nicotine.
Also accelerates gastric acid emptying.

Symptoms
Most  important symptom of peptic ulcer disease is recurrent abdominal pain. Most patients present with recurrent abdominal pain which is mostly localized in the epigastrium.

The pain is usually related to intake of food i.e. the pain occurs intermittently during day and night usually when the stomach is empty and relieves by food. In case of classical duodenal ulcer, the patient is awaken from sleep at late night and gets relief by food, drink or antacid. Ulcer pain is usually episodic and lasts for a few days to weeks in each episode and in between the patient is quite well.

A physician suspects an ulcer when a person presents with characteristic of stomach pain. Symptoms can with the location of the ulcer and the person’s age. For example, children and older people may not have the usual symptoms or may have no symptoms at all. In these instance, ulcers are discovered only when complications develop. Only about half of the people with duodenal ulcers have the typical symptoms of gnawing, burning, aching, soreness, and empty feeling and hunger. The symptoms of gastric, marginal and stress ulcers, unlike those of duodenal ulcers, do not follow any pattern. Gastric ulcers sometimes cause swelling of the tissues (oedema) that lead into the small intestine, which may prevent from easily passing out of the stomach. This blockage may cause bloating, nausea or vomiting after eating.

Complication of peptic ulcers such as bleeding or rupture are accompanied by symptoms of low blood pressure.

Diagnosis
A doctor suspects an ulcer when a person has characteristic of stomach pain. Sometimes the doctor simply treats the person for an ulcer to see if they symptoms resolve, which suggests that the person had an ulcer that has healed.

Tests may be needed to confirm the diagnosis, especially when symptoms do not resolve after a few weeks of treatment because stomach cancer can cause similar symptoms. Also when severe ulcers resist treatment, particularly if a person has several ulcers or the ulcers are in unusual places, a doctor may suspect an underlying condition that causes the stomach to overproduce acid.

Investigations
1. Endoscope of upper GI tract: This is the best diagnostic method, if and when available, endoscopy is used to diagnose ulcers and to determine their cause (a procedure performed using a flexible viewing tube). Endoscopy is more reliable than barium contrast X-rays for detecting ulcers in the duodenum and on the back wall of the stomach.
2. Ba-meal X-ray of stomach and duodenum with cap series may show cap deformity and ulcer crater if ulcer is present.
3. Detection of Helicobacter pylori and cancer cells with an endscope a doctor can perform a biopsy (collection of a tissue sample for examination under a microscope) to determine if a gastric ulcer is cancerous and also to help identify the presence of Helocobactor pylori bacteria.

Treatment
Consist of (1) medical management (2) surgical managements. Medical management with modern medicines such as H2 receptor blockers, proton pump inhibitors etc. and the earlier products like cinetidine ramitidin, famotidine and antacids have wonderful influence in curing ulcers. Chronic unhealed ulcer and complicated ulcers are treated by surgery.

Antacids
Antacids relieve symptoms of ulcers by neutralizing stomach acid. Their effectiveness varies with the amount of antacid taken and the amount of acid a person produces. Almost all antacids can be purchased without a doctor’s prescription and are available in tablet or liquid form. Generally antacids are not effective in healting ulcers.

Ulcers penetrate into the lining of the stomach or duodenum. Gastritis may develop into ulcers. The names given to specific ulcers identify their anatomic locations of the circumstances under which they develop. Duodenal ulcers the most common type of peptic ulcer, occur in the duodenum, the first few inches of small intestine just below the stomach.

Sodium bicarbonate and calcium carbonate, the strongest antacids, may be taken occasionally for short-term relief. However, because they are absorbed by the bloodstream, continual use of these drugs may make the blood too alkaline (alkalosis), resulting in nausea, headache and weakness. Therefore, these antacids generally should not be used in large amounts for more than a few days. These products also contain a lot of salt and should not be used by people who need to follow a low-sodium diet.
Aluminum hydroxide is a relatively safe, commonly used antacid. However, aluminum may bind with phosphate in the digestive tract, reducing phosphate levels in the blood and causing weakness and a loss of appetite. The risk of these side effects is greater in alcoholics and in people with kidney disease, including those receiving dialysis. Aluminum hydroxide may also cause constipation.

Magnesium hydroxide is a more effective antacid than aluminum hydroxide. Bowel movements usually remain regular if only four doses of 1 to 2 tablespoons a day are taken; more than four doses a day may cause diarrhea. Because small amounts of magnesium are absorbed into the blood stream, people with kidney damage should take magnesium hydroxide only in small doses. Many antacids contain both magnesium hydroxide and aluminum hydroxide.

Histamine-2(H) blockers, such as cimetidine, famotidine, nizatidine and ranitidine, relieve symptoms and promote acid. These highly effective drugs are taken once or twice a day. Ha blockers usually do not cause serious side effects, particularly in older people, in whom the drug may cause confusion. In addition, cimetidine may interfere with the body’s elimination of certain drugs such as theophylline for asthama, warfarin for excessive blood clotting and phenytoin for seizures.

Proton pump inhitors are the most potent of the drugs that reduce acid production. Proton pump inhibitors promote healing of ulcers in a greater percentage of people in a shorter period of time than do H blockers. They are also very useful in treating conditions that cause excessive stomach acid secretion, such as Zollinger-Ellison syndrome.

Because infection with H Pylori bacteria is a major cause of ulcers, antibiotics are often used. Sometimes bismuth subsolicylate is used in combination with antibiotics.

Sucralfate may work by forming a protective coating in the base of an ulcer to promote healing. It works well on peptic ulcers and is a reasonable alternative to antacids. Sucralfate is taken 2 to 4 times a day and is not absorbed into the bloodstream, so it cause few side effects. It may however, cause constipation and in some cases it reduces the effectiveness of other drugs.

Misoprostol may be used to reduce the likelihood of developing stomach and duodenal ulcers caused by NSAIDs. Misoprostaol may work by reducing production of stomach acid and by making the stomach lining more resistant to acid. People who are at higher risk of developing an ulcer caused by NSAIDs for other reasons, including older people, people taking corticosteroids and people who have a history of ulcers may also be potential candidates for miscoprostol. However, misoprostol causes diarrhea and other digestive problems in more than 30 of people who take it. In addition, this drug can cause spontaneous abortions in pregnant women. Alternatives to misoprostol are available for people taking aspirin, NSAIDs, or corticosteroids. These alternatives such as proton pump inhibitors, are just as effective for reducing the likelihood of developing an ulcer and cause fewer side effects.

Managements
Aim of management
A. General management for the patient
B. Short-term treatment to relieve symptoms and induce ulcer healing.
C. Long-term or maintenance treatment to prevent relapse

General management
1. Bed rest- during acute exacerbation
2. Diet- a. Regular timing of meals, b. Nutritious diet, c. Irritant and highly spicy food should be avoided, d. Tea, coffee etc. best avoided, e. In acute phase it is often useful to give full liquid or soft diet.
3. Smoking strictly prohibited
4. Steroid, Aspirin and NSAID groups of drugs should be avoided.
The pharmacologic agents that are used in the short-term treatment of peptic ulcers to relieve acute symptoms and enhance the healing are divided into three categories.
1. Acid anti-secretory agents-
Proton pump inhibitors viz. Omearazole
Ha receptor antagonists viz. Cimetidine, Ranitidine, Famotidine and Nizatidine.
2. Mucosal protective agents-
Sucralfate, Bismuth, Misoprostol (a prostaglandin analogue) and antacids.
3. Agents that promote healing through eradication of H. pylori-Proton ump inhibitor (viz. omeprazole, lansoprazole); some antibiotics (e.g amoxicillin clarithromycin, tetracycline) and metronidazole.

Treatment options for peptic ulcer disease
A. Treatment of active ulcer associated with H. pylori
I. Administer Omeprazole 20mg twice daily or Lansoprazole 30mg twice daily with one of the following regimen for 1 week:
a. Metronidazole 400mg 2 times daily + Amoxycillin 500mg 2 times daily. Or
b. Metronidazole 400mg 2 times daily + Clarithromycin 500mg 2 times daily + Clarithromycin 500mg 2 times daily. Or
c. Amoxycillin 500mg 2 times daily + Clarithromycin 500mg 2 times daily. Or
d. Bismuth subsalicylate 125mg 4 times daily + Amoxycillin 500mg 2 times daily + Metronidazole 400mg 2 times daily.

N.B:
i. Some authors advised amoxicillin 1gm instead of 500mg and metronidazole 500mg instead of 400mg and duration 10-14 days instead of 1 week.
ii. Omeprazole must be administered before meal; all antibiotics and Bismuth administered with meal.
iii. Without the eradication of H. pylori, 80 of ulcers will recur within 1 year.
II. After completion of 1 week treatment, continue treatment with proton pump inhibitor (Omeprazole or Lansoprazole) or with Ha receptor blocker for 4-8 weeks to promote ulcer healing.
 
B. Active ulcer not attributatble to H. pylori:
Consider other causes: NSAIDs, acid hyper-secretary states, gastric malignancy.
I. Acid-anti-secretary agents
a. Proton pump inhibitors:
i. Uncomplicated duodenal ulcer: Omeprazole 20mg or Lansoprazole 15mg once daily for 4 weeks
ii. Gastric ulcer or complicated ulcer: Omeprazole 20mg twice daily, or Lansoprazole 30mg once daily, or Pantoprazole 40mg once daily for 6-8 weeks.
Or
b. H2 receptor antagonists:
i. Uncomplicated duodenal unlcer: Cimetidine of 800mg, or Ranitidine 300mg, or Nizatidine 300mg or Famotidine 40mg once daily at bedtime for 6 weeks.
ii. Gastrict ulcer: Cimetidine 400mg twice daily, or Ranitidine 150mg twice daily, or Nizatidine 150mg twice daily or Famotidine 20mg twice daily for 8-12 weeks.
iii. Complicated ulcers: H2 receptor antagonists nor recommended.
II. Drugs enhancing mucosal defense:
1. Sucralfate 1gm 4 times daily for uncomplicated duodenal ulcers.
2. Misoprostol (a synthetic prostaglandin analogue) – Promote ulcer healing by stimulating mucus and bicarbonate secretion and mildily inhibiting acid secretion. It is used solely as a prophylactic agent to prevent NSAID-induced ulcers. Dose: 200mgm 6 hourly for shot duration (4-6 weeks).
3. Bismuth- it promotes ulcer healing by stimulating mucosal bicarbonate and prostaglandin production. Bismuth also acts directly against H. pylori and helps in its eradication. Dose: 125mg 6 hourly for short duration (4-6 weeks)
4. Antacids- Low-dose aluminium and magnesium contaning antacid regimens (120-240 mmol/d) promote ulcer healing through stimulation of gastric mucosal defense not by neutralization of gastric acidity.
Although these are now prescribed mainly for symptomatic relief and are widely used for self medication.
Dose: 15-30ml liquid antacid 2-4 hourly until pain subsided, then 2 tsf (10ml) 1 hour after each meal and at bed time for 4-6 weeks.
III. Supporting treatment:
Diazepam- especially during acute exacerbation when patient become restless (5mg at bed time).
Anticholinergic agents- these agents decrease gastric acid secretion but usually not used.
C. Maintenance treatment to prevent ulcer relapse
a. NSAID induced ulcer prophylactic therapy reserved for high-risk patients (prior ulcer diseases or ulcer complications use of corticosteroids or anticoagulants, age > 70 years), Misoprostal 100-200 mgm 4 times daily.
Or Proton pump inhibitor twice daily (for high-risk patients intolerant of misoprostol)
b. Chronic maintenance therapy: Hg recptor antagonist at bedtime (cimetidine 400-800gm, ranitidine or naxatidine 150-300mg, or famotidine 20-40mg).
Continuous maintenance treatments with small doses of H2-receptor antagonists will prevent ulcer relapse as many as 80 per cent patients remain ulcer free for as long as treatment is maintained. Long-term maintenance treatment with H2-receptor antagonists are safe and effective.

Indications
i. Recurrent ulcers who are with H pylori negative or
ii. Those patients whose H pylori cannot be eradicated or
iii. Patient with history of ulcer complication or
iv. Frequent symptomatic relapse or
v. When surgery is not possible due to other causes.

Surgery
1. When adequate medical measures fails
2. Normal life procedure is hampered
3. Evidence of outlet obstruction or hour glass contracture
4. Repeated haematemesis and malaena not controlled by medical measures.
5. Perforation
6. Possibility of malignancy
7. When ulcer developed in young adult or adolescence

Gastrointestinal Bleeding
Gastrointestinal bleeding or haemorrhage may be divided into two subdivisions, according to the involvement of the part of the g.i tract, viz.
1. Upper gastrointestinal bleeding (upto small intestine or including caecum).
2. Lower gastrointestinal bleeding
According to the site and nature, gastrointestinal bleeding can be divided as-
1. Acute upper gastrointestinal bleeding
2. Severe acute lower gastrointestinal bleeding
3. Subacute or chronic lower gastrointestinal bleeding
4. Chronic or occult gastrointestinal bleeding.

Compiled by Dr. F. I. Biswas