Physiology of Gastrointestinal Disorders

Effective therapy for most gastrointestinal disorders depends on a basic knowledge of gastrointestinal physiology. The purpose of this chapter, therefore, is to discuss a few representative types of gastrointestinal malfunction that have special physiologic bases or consequences.

Disorders of Swallowing and of the Esophagus

Paralysis of the Swallowing Mechanism. Damage to the 5th, 9th, or 10th cerebral nerve can cause paralysis of significant portions of the swallowing mechanism. Also, a few diseases, such as poliomyelitis or encephalitis, can prevent normal swallowing by damaging the swallowing center in the brain stem. Finally, paralysis of the swallowing muscles, as occurs in muscle dystrophy or in failure of neuromuscular transmission in myasthenia gravis or botulism, can also prevent normal swallowing.

When the swallowing mechanism is partially or totally paralyzed, the abnormalities that can occur include (1) complete abrogation of the swallowing act so that swallowing cannot occur, (2) failure of the glottis to close so that food passes into the lungs instead of the esophagus, and (3) failure of the soft palate and uvula to close the posterior nares so that food refluxes into the nose during swallowing.

One of the most serious instances of paralysis of the swallowing mechanism occurs when patients are under deep anesthesia. Often, while on the operating table, they vomit large quantities of materials from the stomach into the pharynx; then, instead of swallowing the materials again, they simply suck them into the trachea because the anesthetic has blocked the reflex mechanism of swallowing. As a result, such patients occasionally choke to death on their own vomitus.

Achalasia and Megaesophagus. Achalasia is a condition in which the lower esophageal sphincter fails to relax during swallowing. As a result, food swallowed into the esophagus then fails to pass from the esophagus into the stomach. Pathological studies have shown damage in the neural network of the myenteric plexus in the lower two thirds of the esophagus. As a result, the musculature of the lower esophagus remains spastically contracted, and the myenteric plexus has lost its ability to transmit a signal to cause "receptive relaxation" of the gastroesophageal sphincter as food approaches this sphincter during swallowing.

When achalasia becomes severe, the esophagus often cannot empty the swallowed food into the stomach for many hours, instead of the few seconds that is the normal time. Over months and years, the esophagus becomes tremendously enlarged until it often can hold as much as 1 liter of food, which often becomes putridly infected during the long periods of esophageal stasis. The infection may also cause ulceration of the esophageal mucosa, sometimes leading to severe substernal pain or even rupture and death. Considerable benefit can be achieved by stretching the lower end of the esophagus by means of a balloon inflated on the end of a swallowed esophageal tube. Antispasmotic drugs (drugs that relax smooth muscle) can also be helpful.

Disorders of the Stomach

Gastritis—Inflammation of the Gastric Mucosa. Mild to moderate chronic gastritis is exceedingly common in the population as a whole, especially in the middle to later years of adult life.

The inflammation of gastritis may be only superficial and therefore not very harmful, or it can penetrate deeply into the gastric mucosa, in many long-standing cases causing almost complete atrophy of the gastric mucosa. In a few cases, gastritis can be acute and severe, with ulcerative excoriation of the stomach mucosa by the stomach's own peptic secretions.

Research suggests that much gastritis is caused by chronic bacterial infection of the gastric mucosa. This often can be treated successfully by an intensive regimen of antibacterial therapy.

In addition, certain ingested irritant substances can be especially damaging to the protective gastric mucosal barrier—that is, to the mucous glands and to the tight epithelial junctions between the gastric lining cells— often leading to severe acute or chronic gastritis. Two of the most common of these substances are excesses of alcohol or aspirin.

Gastric Barrier and Its Penetration in Gastritis. Absorption of food from the stomach directly into the blood is normally slight. This low level of absorption is mainly caused by two specific features of the gastric mucosa: (1) it is lined with highly resistant mucous cells that secrete a viscid and adherent mucus and (2) it has tight junctions between the adjacent epithelial cells. These two together plus other impediments to gastric absorption are called the "gastric barrier."

The gastric barrier normally is resistant enough to diffusion so that even the highly concentrated hydrogen ions of the gastric juice, averaging about 100,000 times the concentration of hydrogen ions in plasma, seldom diffuse even to the slightest extent through the lining mucus as far as the epithelial membrane itself. In gastritis, the permeability of the barrier is greatly increased. The hydrogen ions do then diffuse into the stomach epithelium, creating additional havoc and leading to a vicious circle of progressive stomach mucosal damage and atrophy. It also makes the mucosa susceptible to digestion by the peptic digestive enzymes, thus frequently resulting in gastric ulcer.

Gastric Atrophy. In many people who have chronic gastritis, the mucosa gradually becomes more and more atrophic until little or no gastric gland digestive secretion remains. It is also believed that some people develop autoimmunity against the gastric mucosa, this also leading eventually to gastric atrophy. Loss of the stomach secretions in gastric atrophy leads to achlorhy-dria and, occasionally, to pernicious anemia.

Achlorhydria (and Hypochlorhydria). Achlorhydria means simply that the stomach fails to secrete hydrochloric acid; it is diagnosed when the pH of the gastric secretions fails to decrease below 6.5 after maximal stimulation. Hypochlorhydria means diminished acid secretion. When acid is not secreted, pepsin also usually is not secreted; even when it is, the lack of acid prevents it from functioning because pepsin requires an acid medium for activity.

Pernicious Anemia in Gastric Atrophy. Pernicious anemia is a common accompaniment of gastric atrophy and achlorhydria. Normal gastric secretions contain a glycoprotein called intrinsic factor, secreted by the same parietal cells that secrete hydrochloric acid. Intrinsic factor must be present for adequate absorption of vitamin B12 from the ileum. That is, intrinsic factor com bines with vitamin B12 in the stomach and protects it from being digested and destroyed as it passes into the small intestine. Then, when the intrinsic factor-vitamin B12 complex reaches the terminal ileum, the intrinsic factor binds with receptors on the ileal epithelial surface. This in turn makes it possible for the vitamin B12 to be absorbed.

In the absence of intrinsic factor, only about 1/50 of the vitamin B12 is absorbed. And, without intrinsic factor, an adequate amount of vitamin B12 is not made available from the foods to cause young, newly forming red blood cells to mature in the bone marrow. The result is pernicious anemia. This is discussed in more detail in Chapter 32.

Peptic Ulcer

A peptic ulcer is an excoriated area of stomach or intestinal mucosa caused principally by the digestive action of gastric juice or upper small intestinal secretions. Figure 66-1 shows the points in the gastrointestinal tract at which peptic ulcers most frequently occur, demonstrating that the most frequent site is within a few centimeters of the pylorus. In addition, peptic ulcers frequently occur along the lesser curvature of the antral end of the stomach or, more rarely, in the lower end of the esophagus where stomach juices frequently reflux. A type of peptic ulcer called a marginal ulcer also often occurs wherever a surgical opening such as a gastro-jejunostomy has been made between the stomach and the jejunum of the small intestine.

Basic Cause of Peptic Ulceration. The usual cause of peptic ulceration is an imbalance between the rate of secretion of gastric juice and the degree of protection afforded by (1) the gastroduodenal mucosal barrier and (2) the neutralization of the gastric acid by duodenal juices. It will be recalled that all areas normally exposed to gastric juice are well supplied with mucous glands, beginning with compound mucous glands in the lower esophagus plus the mucous cell coating of the stomach mucosa, the mucous neck cells of the gastric glands, the deep pyloric glands that secrete mainly mucus, and, finally, the glands of Brunner of the upper duodenum, which secrete a highly alkaline mucus.

In addition to the mucus protection of the mucosa, the duodenum is protected by the alkalinity of the small

Cardia

Causes:

1. High acid and peptic content

2. Irritation /

3. Poor blood supply /

4. Poor secretion of mucus Ulcer

5. Infection, H. pylori sites

Pylorus

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Essentials of Human Physiology

Essentials of Human Physiology

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