peptic ulcers?

Question

has anyone ever suffered from them what are the symptoms do you get nausea and feel very ill. I also get burning pain in my abdomen and loss of appetite does anyone else suffer from this???

Answer 1

Symptoms of a peptic ulcer can be:

Abdominal pain, classically epigastric with severity relating to mealtimes (duodenal ulcers are classically relieved by food, while gastric ulcers are exacerbated by it);
Bloating and abdominal fullness
Waterbrash (bitter regurgitation)
Nausea, and sometimes vomiting
Loss of appetite and weight loss;
Hematemesis (vomiting of blood);
Melena (tarry, foul-smelling feces due to oxidised iron from hemoglobin);
Rarely, an ulcer can lead to a gastric or duodenal perforation. This is extremely painful and requires immediate surgery.

peptic ulcer
Peptic ulcer ICD-10 K25-26
ICD-9 531-534

A benign gastric ulcer (from the antrum) of a gastrectomy specimen.
Endoscopic image of gastric ulcer, biopsy proven to be gastric cancer.A peptic ulcer is an ulcer of one of those areas of the gastrointestinal tract that are usually acidic. A more general term, peptic ulcer disease (PUD), is also in use.

Most ulcers are associated with Helicobacter pylori, a spiral-shaped bacterium that lives in the acidic environment of the stomach. Ulcers can also be caused or worsened by drugs such as Aspirin and other NSAIDs. Contrary to general belief, more peptic ulcers arise in the duodenum (=first part of the small intestine, just after the stomach) than in the stomach. About 4 % of stomach ulcers are caused by a malignant tumour, so multiple biopsies are needed to make sure. Duodenal ulcers are generally non-malignant.


Classification
A peptic ulcer may arise at various locations:

Stomach (called gastric ulcer)
Duodenum (called duodenal ulcer)
Esophagus (called esophageal ulcer)
A Meckel's diverticulum

Symptoms and signs
Symptoms of a peptic ulcer can be:

Abdominal pain, classically epigastric with severity relating to mealtimes (duodenal ulcers are classically relieved by food, while gastric ulcers are exacerbated by it);
Bloating and abdominal fullness
Waterbrash (bitter regurgitation)
Nausea, and sometimes vomiting
Loss of appetite and weight loss;
Hematemesis (vomiting of blood);
Melena (tarry, foul-smelling feces due to oxidised iron from hemoglobin);
Rarely, an ulcer can lead to a gastric or duodenal perforation. This is extremely painful and requires immediate surgery.
A history of heartburn, gastroesophageal reflux disease (GERD) and use of certain forms of medication can raise the suspicion for peptic ulcer. Medicines associated with peptic ulcer include NSAID (non-steroid anti-inflammatory drugs) that inhibit cyclooxygenase, and most glucocorticoids (e.g. dexamethasone and prednisolone).

In patients over 45 with more than 2 weeks of the above symptoms the odds for peptic ulceration are high enough to warrant rapid investigation by EGD (see below).

The timing of the symptoms in relation to the meal may differentiate between gastric and duodenal ulcers: A gastric ulcer would give epigastric pain during the meal, as gastric acid is secreted, or after the meal, as the alkaline duodenal contents reflux into the stomach. Symptoms of duodenal ulcers would manifest mostly before the meal — when acid (production stimulated by hunger) is passed into the duodenum.


Stress and ulcers
Despite the finding that a bacterial infection is the cause of ulcers in 75% of cases, support for the theory that stress causes ulcers has not disappeared.

An expert panel convened by the Academy of Behavioral Medicine research concluded that ulcers are not merely an infectious disease and that psychological factors do play a significant role. [2]

One researcher said,

Having a positive attitude seems to correlate with an increased ability of the immune system in fighting diseases.[3]
According to research physician Susan Levenstein,

I have a suspicion that one reason the medical establishment wiped stress off the charts so fast was that it didn't feel comfortable with psychological explanations. They were happier when they could label ulcers as an infectious disease. It's easy to fall into either-or thinking: either ulcers are caused by stress or they're caused by Helicobacter. The truth is much more complicated and, I think, more exciting. Since peptic ulcer is one of the few 'infectious' diseases in which stress plays an important role, it gives us a great model for understanding how psychological factors can tip the balance toward disease, in the uneasy equilibrium we all live in with a whole variety of infectious agents. [4]
The discovery that Helicobacter pylori is a cause of peptic ulcer has tempted many to conclude that psychological factors are unimportant. But this is dichotomised thinking. There is solid evidence that psychological stress triggers many ulcers and impairs response to treatment, while helicobacter is inadequate as a monocausal explanation as most infected people do not develop ulcers. Psychological stress probably functions most often as a cofactor with H pylori. It may act by stimulating the production of gastric acid or by promoting behaviour that causes a risk to health. Unravelling the aetiology of peptic ulcer will make an important contribution to the biopsychosocial model of disease. [5]

Pathophysiology
Tobacco smoking, blood group, spices and other factors that were suspected to cause ulcers until late in the 20th century, are actually of relatively minor importance in the development of peptic ulcers.[1]

A major causative factor (75% of gastric and 90% of duodenal ulcers) is chronic inflammation due to Helicobacter pylori, which appears spiral, but is not a spirochaete, rather a bacillus, that colonizes (i.e. settles there after entering the body) the antral mucosa. The immune system is unable to clear the infection[2], despite the appearance of antibodies. Thus, the bacterium can cause a chronic active gastritis (type B gastritis), resulting in a defect in the regulation of gastrin production by that part of the stomach, and gastrin secretion is increased. Gastrin, in turn, stimulates the production of gastric acid by parietal cells. The acids erodes the mucosa and causes the ulcer.

Another major cause is the use of NSAIDs (see above). The gastric mucosa protects itself from gastric acid with a layer of mucous, the secretion of which is stimulated by certain prostaglandins. NSAIDs block the function of cyclooxygenase 1 (cox-1), which is essential for the production of these prostaglandins. Newer NSAIDs (celecoxib, rofecoxib) only inhibit cox-2, which is less essential in the gastric mucosa, and roughly halve the risk of NSAID-related gastric ulceration.

Glucocorticoids lead to atrophy of all epithelial tissues. Their role in ulcerogenesis is relatively small.

Stress in the psychological sense has not been proven to influence the development of peptic ulcers.[3] Burns and head trauma, however, can lead to "stress ulcers", and it is reported in many patients who are on mechanical ventilation.

Smoking leads to atherosclerosis and vascular spasms, causing vascular insufficiency and promoting the development of ulcers through ischemia.

A family history is often present in duodenal ulcers, especially when blood group O is also present. Inheritance appears to be unimportant in gastric ulcers.

Gastrinomas (Zollinger Ellison syndrome), rare gastrin secreting tumors, cause multiple and difficult to heal ulcers.


Diagnosis
An esophagogastroduodenoscopy (EGD), a form of endoscopy, also known as a gastroscopy, is carried out on patients in whom a peptic ulcer is suspected. By direct visual identification, the location and severity of an ulcer can be described. Moreover, if no ulcer is present, EGD can often provide an alternative diagnosis.

The diagnosis of Helicobacter pylori can be by:

Biopsy during EGD;
Breath testing (does not require EGD);
Direct culture from an EGD biopsy specimen;
Direct detection of urease activity in a biopsy specimen;
Measurement of antibody levels in blood (does not require EGD). It is still somewhat controversial whether a positive antibody without EGD is enough to warrant eradication therapy.
The possibility of other causes of ulcers, notably malignancy (gastric cancer) needs to be kept in mind. This is especially true in ulcers of the greater (large) curvature of the stomach; most are also a consequence of chronic H. pylori infection.

If a peptic ulcer perforates, air will leak from the inside of the gastrointestinal tract (which always contains some air) to the peritoneal cavity (which normally never contains air). This leads to "free gas" within the peritoneal cavity. If the patient stands erect, as when having a chest X-ray, the gas will float to a position underneath the diaphragm. Therefore, gas in the peritoneal cavity, shown on an erect chest X-ray or supine lateral abdominal X-ray, is an omen of perforated peptic ulcer disease.


Macroscopical appearance
Gastric ulcer is most often localized on the lesser curvature of the stomach. It is a round to oval parietal defect ("hole"), 2 to 4 cm diameter, with a smooth base and perpendicular borders. These borders are not elevated or irreguliar as in gastric cancer - ulcerative form. Surrounding mucosa may present radial folds, as a consequence of the parietal scarring.


Microscopical appearance
Gastric peptic ulcer is a mucosal defect which penetrates the muscularis mucosae and muscularis propria, produced by acid-pepsin aggression. Ulcer margins are perpendicular and present chronic gastritis. During the active phase, the base of the ulcer shows 4 zones: inflammatory exudate, fibrinoid necrosis, granulation tissue and fibrous tissue. The fibrous base of the ulcer may contain vessels with thickened wall or with thrombosis. 1


Treatment

Younger patients with ulcer-like symptoms are often treated with antacids or H2 antagonists before EGD is undertaken. Bismuth compounds may actually reduce or even clear organisms.

Patients who are taking nonsteroidal anti-inflammatories (NSAIDs) may also be prescribed a prostaglandin analogue (Misoprostol) in order to help prevent peptic ulcers, which may be a side-effect of the NSAIDs.

When H. pylori infection is present, the most effective treatments are combinations of 2 antibiotics (e.g. Erythromycin, Ampicillin, Amoxicillin, Tetracycline, Metronidazole) and 1 proton pump inhibitor (PPI). An effective combination would be Amoxicillin + Metronidazole + Pantoprazole (a PPI). In the absence of H. pylori, long-term higher dose PPIs are often used.

Treatment of Helicobacter usually leads to clearing of infection, relief of symptoms and eventual healing of ulcers. Recurrence of infection can occur and retreatment may be required, if necessary with other antibiotics. Since the widespread use of PPI's in the 1990s, surgical procedures (like "highly selective vagotomy") for uncomplicated peptic ulcers became obsolete.

Perforated peptic ulcer is a surgical emergency and requires surgical repair of the perforation. Most bleeding ulcers require endoscopy urgently to stop bleeding with cautery or injection.

Answer 2

I wouldnt think so. And 1 joint doesnt equal 20 cigarettes damn people are dumb. I supposedly equals 4. But the stuff in cigarettes such as tar and poisons is whats bad about it. Id ask a doctor though just give them a call.

Answer 3

burning pain in stomach after eating food.