The GIT breaks down foods by first using mechanical means such as chewing and then by the application of a host of complex chemical processes. These chemical processes include everything from saliva to colon microbes. Since the GIT is the point of entry for the human body, everything eaten has an impact on the body. The food eaten and passed through the GIT contains nutrients as well as toxins. Toxins can be anything from food additives and pesticides to specific foods that induce a reaction from the GIT.
The process of digestion is accomplished via the surface of the GIT using secretions from accessory glands. The two glands providing the majority of digestive chemicals utilized by the GIT are the liver and the pancreas. The function of the liver is to control the food supply for the rest of the body by further processing the food molecules absorbed through the intestines. The liver does this by dispensing those food molecules in a controlled manner and by filtering out toxins that may have passed through the GIT wall. Another very important function of the GIT is as a sensory organ. By rejecting foods through objectionable taste, vomiting, and diarrhea, or any combination of these symptoms, the sensing capacity of the GIT can protect the body.
The surface of the GIT has a complex system of nerves and other cells of the immune system. The surface of the GIT, or mucosa, is part of a complex sensing system called the MALT (mucosa-associated lymphatic tissue). The immune sensors in MALT trigger responses such as nausea, vomiting, pain, and swelling. Vomiting and diarrhea are abrupt defensive responses by MALT when it senses foods with a strong allergic or toxic component. This kind of food intolerance is responsible for many digestive problems. The GIT is "hard-wired" to the brain via hormonal, neurotransmitter-mediator chemical communication.
A peptic ulcer is a hole in the gut lining of the stomach, duodenum, or esophagus. A peptic ulcer of the stomach is called a gastric ulcer; of the duodenum, a duodenal ulcer; and of the esophagus, an esophageal ulcer. An ulcer occurs when the lining of these organs is corroded by the acidic digestive juices which are secreted by the stomach cells. Peptic ulcer disease is common, affecting millions of Americans yearly.
The leading cause of ulcer disease is currently believed to be infection of the stomach by a bacteria called "Helicobacter pyloridus" (H. pylori). Another major cause of ulcers is the chronic use of anti-inflammatory medications, commonly referred to as NSAIDs (nonsteroidal anti-inflammatory drugs), including aspirin. Cigarette smoking is also an important cause of ulcer formation and ulcer treatment failure.
H. pylori bacteria is very common, infecting more than a billion people worldwide. It is estimated that half of the United States population older than age 60 has been infected with H. pylori. Infection usually persists for many years, leading to ulcer disease in 10 % to 15% of those infected. H. pylori is found in more than 80% of patients with gastric and duodenal ulcers. While the mechanism of how H. pylori causes ulcers is not well understood, elimination of this bacteria by antibiotics has clearly been shown to heal ulcers and prevent ulcer recurrence.
Many ulcer patients experience minimal indigestion or no discomfort at all. The diagnosis of an ulcer is usually made by an upper endoscopy, which involves sedation of the patient and the insertion of a flexible tube through the mouth to inspect the stomach, esophagus, and duodenum. Upper endoscopy has the added advantage of having the capability of removing small tissue samples (biopsies) to test for H. pylori infection.
Histamine antagonists (H2 blockers) are drugs designed to block the action of histamine on gastric cells, hence reducing acid output. Examples of H2 blockers are cimetidine (Tagamet), ranitidine (Zantac), nizatidine (Axid), and famotidine (Pepcid). While H2 blockers are effective in ulcer healing, they have limited role in eradicating H. pylori without antibiotics. Therefore, ulcers frequently return when H2 blockers are stopped.
Gastroesophageal reflux disease (GERD) is a more serious form of common gastroesophageal reflux (GER). GER occurs when the lower esophageal sphincter opens spontaneously or does not close properly and stomach contents rise up into the esophagus. GER is also called acid reflux because digestive juices rise up with the food.
When acid reflux occurs, food or fluid can be tasted in the back of the mouth. When refluxed stomach acid touches the lining of the esophagus it may cause a burning sensation in the chest or throat called heartburn or acid indigestion. Occasional GER is common and does not necessarily mean one has GERD. Persistent reflux that occurs more than twice a week is considered GERD, and it can eventually lead to more serious health problems.
People of all ages can have GERD. The main symptom of GERD in adults is frequent heartburn, also called acid indigestion—burning-type pain in the lower part of the mid-chest, behind the breast bone, and in the mid-abdomen. Most children under 12 (and some adults) have GERD without heartburn. Instead they may experience a dry cough, asthma symptoms, or trouble swallowing.
Depending on the severity of your GERD, treatment may involve lifestyle changes, medications, or surgery. Your health care provider may recommend over-the-counter antacids or medications that stop acid production or help the muscles that empty your stomach. Because drugs work in different ways, combinations of medications may help control symptoms. People who get heartburn after eating may take both antacids and H2 blockers. The antacids work first to neutralize the acid in the stomach, and then the H2 blockers act on acid production. By the time the antacid stops working, the H2 blocker will have stopped acid production.
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