In the previous minicourse we discovered how the stomach is involved in the digestive process. This minicourse deals with the structure and function of the intestines - both small and large. Most of the digestion and absorption of food takes place in the small intestine, whereas the large intestine is intimately involved with water and electrolyte balance as well as with the absorption of some vitamins. Understanding these important structures is a necessary prerequisite for anyone who will be involved in the treatment of patients having intestinal disorders.
On completion of this minicourse you will be able to:
OBJ. 1. Describe the small intestine in terms of:
The Small Intestine
From the pyloric portion of the stomach, a small muscular valve, the pyloric sphincter, opens into the small intestine. The small intestine, composed of three segments, is about 1 to 1 inches in diameter and approximately 20 feet long (of course this varies with age and with the state of muscular contraction or relaxation).
Although some digestion has already begun (i.e., the mouth and its salivary amylase - initiating carbohydrate digestion; the stomach's pepsin - initiating protein digestion), the majority of digestion and absorption of foodstuffs takes place chiefly in the convoluted tube of the small intestine.
The first portion of the small intestine is called the duodenum. This part extends from the pyloric sphincter toward the right. Following some twisting and turning, it finally winds up on the left side of the body. This twisting and turning causes the duodenum to come near the head of the pancreas, which is one of the digestive glands from which the small intestine receives secretory enzymes (carboxy peptidase, amylase, trypsin, chymotrypsin, lipase, ribonuclease and deoxyribonuclease). It should also be noted that near the center of the duodenum are located the tubular ducts from the liver, gallbladder, and pancreas.
The next part of the small intestine is called the jejunum, and the third is called the ileum. Except by close internal histological inspection, these two parts cannot be readily separated. Together the jejunum and the ileum contribute more than 15 feet to the small intestinal length.
The ileum ends by opening into the large intestine, or colon, via the ileocecal junction. The junction is located in the lower right quadrant of the abdominal cavity. At this junction is the ileocolic sphincter.
It may be helpful to review how much digestion has alreadv taken place before material enters the small intestine. In summary, therefore:
Region Carbohydrates Proteins Fats Mouth Salivary amylase (salivary amylase) breaks starches into monosaccharides and dextrins Stomach Some diestion may Pepsin breaks (pepsin-HCl) continue by salivary proteins into amylase peptones and proteases To small intestine To small To small intestine intestine
You will reca]l that when food is sufficientlv liquified in the stoach (into chyme), it is transported to the small intestine via the pyloric sphincter. As this occurs, the presence of fats within the duodenum causes cholecystokinin and secretin to he released which will inhibit further astric activity. While the chvme is present within the small intestine, glands within this structure begin to secrete different types of digestive enzymes called carbohydrases (amylase, proteases, and lipases or fat splitting r enzymes). The glands responsible for these enzymatic secretions are really pits (found in the mucosal layer of the small intestine) called the crypts of Lieberkuhn. Another set of glands called Brunner's glands are responsible for the secretion of mucus. Collectivey, the intestinal secretions are referred to as succus entericus.
Figure 1 depicts the important anatomical relationship between the duodenum and the liver and pancreas. Secretions from each structure (liver and pancreas) empty into the duodenum. Figure 1
Bile, an olive-green liquid produced in the liver at the rate of 250-1000 ml/day, is composed of bile salts, phospholipids, cholesterol, water, and two important pigments: bilirubin and biliverdin. Bile is usually prevented from reaching the duodenum because of a muscular valve (sphincter) at the opening of the bile duct which is kept closed. There, as bile collects within the bile duct, it will eventually back up and collect within a reservoir structure called the gallbladder. Bile contains bile salts which aid in the digestion of fats through a process called emulsification. Therefore, another action of the presence of fats within the duodenum causing the release of cholecystokinin becomes important. This hormone causes ejection of bile from the gallbladder (by causing gallbladder contraction) and opening of the valve between the common bile duct and the duodenum (sphincter of Oddi).
The bile salts coat the surfaces of fat droplets. This keeps the droplets separated from each other and allows the fat-splitting lipases coming from various sources to break up the large fatty molecules.
An earlier paragraph mentioned the importance of fat to hormonal regulation and secretion. The acidity of chyme is just as important. This acidity, caused by both HCl and by products of protein digestion from the stomach, will stimulate the secretion of the duodenal hormone secretin which causes secretion of bicarbonate-rich pancreatic juice to promote acid neutralization.
The secretions of the pancreas are coming from the exocrine portion (not the endocrine portion, which produces insulin). Therefore, the enzyme-rich pancreatic juice contains:
The important proteases from the pancreas are trypsin and chymotrypsin. Like pepsin from the stomach, trypsin and chymotrypsin are first produced in an inactive form. Thus, trypsin is produced as trypsinogen, which is activated by a protease called enterokinase. Once enterokinase has converted trypsinogen to trypsin, trypsin (a protease) in turn activates another substance, chymotrypsinogen and converts it to chymotrypsin. (If you have managed to keep that straight you are doing well.)
Remember that, under normal conditions, the walls of the stomach and small intestine are coated with a protective mucous film. In cases where this protection is incomplete, digestion of the gastric or duodenal wall can result. This can lead to the production of gastric or duodenal ulcers.
The pancreatic secretion is under hormonal control by secretin and cholecystokinin, both of which are produced by the duodenum.
The results of the digestive process are summarized below:
Carbohydrates Proteins Fats sugars amino acids glycerol fatty acids
Once all this digestion has taken place, the next task for the body becomes one of absorbing these sugars, amino acids, glycerol and fatty acids. The small intestine has been especially modified for this absorptive process. The predominant modification is in the form of villi (finger-like projections) which vastly increase the surface area of the intestine. Embedded within the underlying connective tissue of each villus are an artery, a venule, and a specialized lymphatic vessel called a lacteal. Other modifications for absorption in the small intestine include the microvilli and plicae circulares, both of which further increase the intestinal surface area.
The products of carbohydrate and protein digestion enter the villi of the intestinal lining and are absorbed directly into the bloodstream. From this point they are carried to the hepatic portal system of the liver. On the other hand, the end products of fat digestion (glycerol and fatty acids) are picked up by the specialized lymphatic vessels called lacteals.
Food materials within the small intestine are moved along by peristaltic contractions. These contractions are dependent upon action of the smooth involuntary musculature.
Mouth Stomach Small Intestine Villi Carbohydrates Salivary amylase Some digestion may Pancreatic amylase, breaks starches continue via maltase, lactase into monosacchar- salivary amylase sucrase continue to ides, disaccharides facilitate break- and dextrin down of sugars to monosaccharides: l) glucose 2) fructose 3) glactose Proteins Pepsin breaks Trypsin and chymo- Picked up by villi; proteins into trypsin degrades the then to capillaries peptones and proteins missed in then to hepatic proteses stomach. The pep- portal blood and tones and proteses finally to the liver are further broken down to amino acids Fats Bile and pancreatic Picked up by special- lipase break fats ized lymph vessels down into glycerol called lacteals and fatty acids
OBJECTIVE 1 - Questions
1. Describe the major secretions of the small intestine.
2. Briefly describe how carbohydrates, proteins, and fats are handled during the digestive process.
EXERCISE 1 DISCUSSION
OBJECTIVE 1 - Answers
1. The secretions of the small intestine are called the succus entericus. Brunner's glands secrete mucus. Other glands, the crypts of Lieberkuhn, secrete the carbohydrases, proteases and lipases which are the major digestive enzymes of the small intestine. These glands are located in the mucosal layers of the small intestine.
2. Carbohydrate. About 50% of the starches are digested by amylase from the salivary glands while the starches are in the stomach. Maltose is the primary product of this action. The remaining 50% is broken down into disaccharides and monosaccharides by enzymes (carbohydrases) of the small intestine. Carbohydrates are almost completely absorbed in the jejunum.
Protein. Proteins are broken down into peptides by pepsin and by the enzymes of the pancreas. These peptide fragments are further digested to free amino acids by carboxypeptidase from the intestinal villi. About 70% to 80% of the ingested protein is absorbed by the end of the jejunum.
Fats. Most fat digestion occurs in the small intestine through the
action of pancreatic lipase. Bile salts secreted by the liver speed up
lipid digestion by increasing the surface area (emulsification) of the r-
lipid droplets accessible to the lipase. As digestion proceeds, the bile
salts perform a second important function in promoting aggregation of the
liberated materials into micelles of several thousand molecules. These
micelles are water soluble. During their passage through the intestinal
epithelial cells, the fatty acids are resynthesized into triglycerides
which are released into the lacteals of the lymphatic system.
OBJ. 2. Describe the large intestine in terms of:
a) principal function
b) principal secretions
c) phases of colonic activity
Click here for a radiology study of the colon
The large intestine, which begins at the ileocecal sphincter
(ileocolic junction) and terminates at the anus, is a muscular tube
approximately five feet long and two and one-half inches in diameter. The
first portion of the colon is called the cecum. The small intestine
communicates with the cecum (a blind pouch) via the ileocecal sphincter, which
has two important functions:
1) allows substances to pass from the small intestine to the large intestine
2) prevents substances from moving back into the small intestine
Dangling down from the cecum is a small coiled tube called the vermiform appendix. An infection of this structure can lead to appendicitis.
The cecum opens into the colon (large intestine). Traveling up the right lateral aspect of the abdominal cavity as the ascending colon, it reaches the liver "right turn", also called the "hepatic flexure." Continuing across the abdominal cavity, this part of the colon is called the transverse colon. It continues to the area of the spleen and turns right again to become the descending colon.
At the left iliac crest the descending colon becomes contorted to form the S-shaped sigmoid colon. The tail-end of the S projects toward the midline to form the rectum. This structure lies just anterior to the sacrum and the coccyx. The last two or three centimeters of the rectum are modified into anal columns which are longitudinally arranged arteries and veins. This area is quite delicate. An enlargement and/or inflammation of these veins is called hemorrhoids.
The functions of the large intestine include movement of intestinal contents, absorption of water, vitamins and electrolytes and the formation of feces. As food passes through the ileocecal sphincter, it fills the pouch- like cecum and accumulates within the ascending colon. The digested material is moved by a mechanism called haustral churning. This occurs by filling of a haustrum (out-pocket) to its maximum, followed by a haustral contraction, followed by a filling of a succeeding haustrum. Another mechanism involved in the movement of material through the large intestine is peristalsis. In addition, there is a massive peristaltic contraction, thought to occur three or four times a day, which pushes chyme (feces at this point) from the colon into the rectum. The absorption of food performed by the large intestine is minimal. By the time chyme reaches the large intestine, most of the digestion and absorption is already complete. The chyme, after remaining within the large intestine for five to ten hours, becomes a semisolid mass called feces, which consist of:
Following the action of bacteria, chyme is prepared for elimination. Bacteria normally present within the large intestine perform the following functions:
The large intestine plays an important role in water balance in that it absorbs a considerable quantity of water and electrolytes (particularly sodium). This absorption occurs for the most part in the cecum and ascending colon. It also absorbs products of bacterial action, including inorganic solutes as well as some vitamins.
Objective 3. Describe the circulation of the abdominal region.
When one views the circulatory pattern of the abdominal region, it appears to be very complex. However, this complexity is due primarily to the branching and sub-branching of three main structures which project from the abdominal aorta. These are the celiac, the superior mesenteric, and the inferior mesenteric arteries. The superior mesenteric artery and the inferior mesenteric artery leave the aorta and enter the mesentery that attaches the gut tube to the abdominal wall. While they are in the mesentery they break up into a series of branches that form arterial arcades. These interconnecting arcades provide a collateral circulation for large segments of the bowel. The small arteries that come off the arcades and go directly to the bowel wall do not anastomose after they reach the bowel wall.
Celiac artery hepatic) stomach (Branches at T-12 splenic liver above level of left gastric gallbladder pancreas) pancreas spleen duodenum (to be discussed in the next minicourse) Superior mesenteric Its branches supply artery small intestine appendix, cecum, first 2/3 of colon Inferior mesenteric Supplies the descending and sigmoid colon, and the rectum
You will recall that the venous drainage of this area, as has already been mentioned, brings digested foodstuffs to the liver before they are carried to the heart. The veins draining this area are tributaries to the portal vein which enters the substance of the liver and branches into the interlobular veins which supply the sinusoids of the liver.
Describe the circulation of the bowel in general terms.
The intestine is supplied primarily by medium-sized arteries
that are branches of the aorta. There are two major branches, the superior
mesenteric artery and the inferior mesenteric artery. These leave the aorta
and enter the mesentery that attaches the gut tube to the abdominal wall.
While they are in the mesentery they break up into a series of branches that
form arterial arcades. These interconnecting arcades provide a collateral
circulation for large segments of the bowel. The small arteries that come
off the arcades and go directly to the bowel wall do not anastomose after they
reach the bowel wall.
OBJ. 4. Describe the principal factors involved in normal peristalsis of the intestines.
The gut tract is innervated by extrinsic nerves and intrinsic nerves. The extrinsic nerves are vagus (motor and sensory), sympathetic (motor) and visceral sensory. The vagus motor nerves activate the gut and the vagus sensory nerves are involved in the various reflex arcs necessary for coordinated digestive activity. The sympathetic nerves act to inhibit gut activity. The visceral sensory nerves are segmental nerves from the spinal cord that are primarily composed of pain fibers. In addition, they have receptors for pressure and movement.
The extrinsic motor nerves (vagus) do not end directly on the smooth muscle cells of the gut wall, but rather terminate on a series of ganglion cells in the gut wall. These ganglion cells are called the enteric ganglia, or plexuses. The enteric ganglion cells send their fibers (postganglionic) to the smooth muscle cells. The enteric ganglia and the intestinal smooth muscle are capable of activity without being stimulated by the vagus. All smooth muscle of the gut has intrinsic innervation and ganglia.
As described earlier, peristalsis is a wave-like action which normally passes distally, or in an anal direction. (Reverse peristalsis can occur, however, in response to an abnormal condition.) Peristalsis is initiated when the lumen of the gut is distended and activates the enteric plexus/ganglia complex which stimulates the smooth muscle cells of the gut. The coordinated, rhythmical peristaltic action is a function of the vagus motor and sensory nerves and the sympathetic motor nerves which respond to pressure and movement.
When the food passes a given location, the pressure on the lumen ceases and the peristaltic action proximal to that location ceases.
Most peristaltic activity of the intestine is mediated via the central nervous system through reflex arcs involving the vagus nerve. These depend on the intrinsic nerves of the intestinal wall for their effect on the smooth muscle cell. The entrance of food into the intestine slightly distends the intestine and it reflexly begins a series of contractions that result in a peristaltic wave. The wave is propagated by the ganglion cells in the gut wall. The majority of intestinal activity is probably mediated by mechanical factors rather than hormonal. This is somewhat different from gastric motility which is influenced by gastric and duodenal secretions.
As with most clinical situations, one must have a sound working knowledge of basic anatomy because such knowledge insures a greater understanding of the presenting pathophysiology.
One type of intestinal obstruction is called an intussusception. This condition is characterized by a "telescoping" of one segment of bowel over another. The specific name given to an intussusception depends on the region or regions of the bowel involved. One type of intussusception is described below.
Normally, the ileum at the ileocecal sphincter is found to project slightly into the cecum. Under certain conditions, this inward projection may form the starting point of an invagination of the small intestine into the cecum. This condition, known as an ileocecal intussusception, is progressive in that the invaginated small intestine moves further and further into the ascending colon. By doing so, it drags with it the cecum and the appendix as well as the mesentery and blood supply to the cecum and to the small intestine. As one would suspect, necrosis of the invaginated segment will eventually develop. It should be further noted that this condition is more common in young children than it is in adults.
Another situation which may lead to intestinal obstruction is rotation of the small intestine in a clockwise direction. This condition is referred to as a volvulus. In this condition, the cecum becomes twisted around its long axis. It has been shown that this condition occurs when the cecum and colon are not firmly attached to the abdominal wall. Sometimes the rotation may continue until the blood supply to the gut is completely cut off.
Finally, another condition which may cause gastrointestinal obstruction is carcinoma. Obstruction due to carcinoma occurs because the malignant growth grows both inward and outward. The inward growth creates a direct obstruction whereas the outward growth can, from the lack of space in which to expand, further compromise the lumen as a result of inward pressure on the gut. This condition is more common in persons 50 years or older.
It has been shown that the malignancy is, for an initial period restricted to the bowel wall. Eventually, metastases occur via the lymphatics. As with any cancer, early diagnosis and treatment are very important. In cancer of this region, a partial colectomy accompanied by removal of lymph vessels and nodes promotes the possibility of successful recovery.
These problems will be investigated from a clinical viewpoint in a future minicourse.
Describe the three types of intestinal obstruction which were presented in this minicourse.
OBJ. 7. Describe the two most common positions of the appendix.
OBJ. 8. Describe the pathophysiology of acute appendicitis.
Hanging from the cecum is a small organ containing a large amount of lymphatic tissue. This worm-like structure, about three to five inches long, is called the vermiform appendix. It is located just below the ileocolic junction on the posteromedial aspect of the cecum. The appendix has a mesentery of its own called the mesoappendix. It is really a portion of the mesentery attachment to the small intestine. Thus, the appendix can be considered to be freely mobile, because the mesoappendix exerts very little restraint. It is not uncommon for the lower one-third of the structure to be devoid of mesentery, thus adding to its mobility. The appendix is located in the right lower quadrant beneath McBurney's point.
The end of the appendix, which is devoid of mesentery, is thus highly movable and may adopt various positions depending on its attachment to the cecum. Following is a list of the most common positions:
The arterial supply to the appendix is via a branch of the posterior cecal artery known as the appendicular artery. The posterior cecal vein drains the appendix.
The appendix has a large amount of lymphatic tissue. Because of this, it is conjectured that this organ may be involved in the immunological process. The lymph that is drained from this structure eventually reaches the superior mesenteric nodes.
The appendix, it should be remembered, is a blind tube which hangs down from the cecum. Because of this, it accumulates food and bacteria. Normally, this is not a problem. Sometimes, however, the appendiceal-cecal orifice, which is the attachment of the appendix to the cecum, becomes occluded. Because of this the structure cannot cleanse itself. Inflammation may result leading to pain in the right lower quadrant. In most instances surgery is recommended because appendicular rupture could result in peritonitis.
As describe above, obstruction of the appendiceal lumen can lead to a condition called acute appendicitis. Interference with the vascular supply to the structure, however, may be another causative factor. These two etiological factors probably cause the wall of the appendix to lose its ability to resist the invasion of bacteria which are potential pathogens. Some of the more common organisms found within the diseased appendix are various streptococci as well as the bacilli normally found in the colon. Acute appendicitis can be classified as follows:
The more salient points concerning the pathophysiology of acute appendicitis are as follows:
OBJ 9. Describe the physiological basis of intestinal motility and its effects on water and electrolyte balance.
OBJ. 10. Describe common dysfunctions of the intestinal tract and the effects of laxatives, cathartics and antidiarrheal agents on those dysfunctions.
Normal swallowing is accomplished by peristaltic movements. These are initiated by reflexes arising from voluntary contractions of the muscles of the pharynx. As the food bolus is pressed against the posterior pharyngeal wall the pressure in the pharynx rises and the muscles contract to seal off the larynx. The contractions of the Laryngeal muscles pushes the food bolus downward into the esophagus which has a lower pressure. The wave of contraction thus initiated voluntarily sweeps down the esophagus, propelling the food bolus along. This reflex is subserved by the voluntary system in the mouth, pharynx and upper one-third of the esophagus. The contraction wave in the lower two-thirds of the esophagus is an autonomic reflex (parasympathetic - vagus). During this process the larynx is elevated against the epiglottis and the posterior wall of the pharynx moves forward to complete sealing off the laryngeal opening. The soft palate is also reflexively elevated and comes in apposition to the advancing posterior pharyngeal wall to seal off the nose.
Dysphagia (difficulty in swallowing) may result from a defect or disorder in any part of the above mechanisms. Mechanical obstruction may also interfere with propelling the food bolus. Emotional conflicts in a patient may also interfere with the function of this system. The motility of the lower esophagus may be altered by disease processes in the muscular wall or diseases that interfere with the intrinsic nervous system (diseases that either paralyze it or erode it so that there are breaks in its continuity).
As food bolus enters the stomach, a small amount is propelled on through the stomach into the duodenum. This apparently acts as a signal for the pyloric sphincter to close. During the quiescent phases, the pyloric sphincter is relaxed. It contracts in response to acidic stomach contents reaching the duodenum.
The remainder of the ingested food enters the stomach, which dilates progressively to accommodate the food. There now follows a period of propulsive churning movements. Next, a series of peristaltic waves begins near the pyloric end of the stomach and continues over the duodenal wall. These waves also begin to extend up onto the body of the stomach. They continue until the stomach is empty, at which point all activity ceases. Except when there is a very large intake of food, most of the passage of food and churning action takes place along the lesser curvature. The lesser curvature, called magenstrasse (great street), is the area of most of the gastric activity. Recall the prominence of ulcers along the lesser curvature.
Gastric emptying is retarded when the duodenum receives low pH solutions or hypertonic solutions of sugar, sodium chloride or fats. Gastric emptying is accelerated, however, by the administration of alkaline solutions.
Vigorous peristaltic activity of the stomach is associated with normal hunger. Nausea is accompanied by a cessation of gastric activity and simultaneous sustained contraction of the duodenum. That the reactions of nausea and hunger are mediated by the central nervous system is evidenced by the fact that they both occur in the gastrectomized patient.
Motility of the intestinal tract may vary from a hypermotive phase to a hypomotile phase to a complete cessation of activity. These changes in normal colonic function may be induced by emotional stress, humoral agents, defective innervation (both motor and sensory), diseases in other systems and intrinsic disease of the colon itself.
The colon has two main functions, the absorption of water and crystalloids and the storage of fecal material until it can be evacuated. The material that enters the colon from the ileum is a highly fluid mass. Most of the activity of the colon is a slow, phasic, kneading type of contraction which facilitates absorption. At periodic intervals, usually after a meal, a period of mass peristalsis occurs which moves the colonic contents into the rectum. Interference with intestinal motility will interfere with the normal functions of the colon, especially the function of water resorption. This causes a highly fluid fecal mass which fills and distends the rectum and causes the defecation reflex to occur.
Dysfunction of the colon may also cause excessively long retention of the fecal material, resulting in constipation.
Dysfunction of the colon upsets the transfer of water across the various membranes. Here also the passage of water is by passive osmotic diffusion and depends on the various other osmotic pressures exerted across the membrane. Abnormal activity of the colon (either hyper or hypo) affects this diffusion process in several ways. It affects the passage of water across the intestinal mucosa, from the interstitial fluid of the colon and alters the exchange of fluid across the capillary beds of the colon.
The loss of large amounts of fluid in diarrhea causes a shifting of the water and electrolyte balance in the various compartments of the body.
Fluid lost into the lumen of the gut due to dysfunction of the mucosa and muscularis layers is drawn from the interstitial spaces of the colon, which upsets the fluid exchange at the capillary bed. This causes fluid to leave the plasma and enter the interstitial spaces of the colon. Recall that ionic transfer is also passive and occurs in the direction of fluid flow. Therefore, loss of fluid into the lumen of the colon causes both water and electrolytes to leave the blood and enter the tissue spaces to be ultimately lost across the colonic membranes into the lumen. As the blood electrolyte supply is depleted, other water and electrolyte stores in the body begin to release fluid and ions into the plasma in an attempt to restore equilibrium. Nausea is an unpleasant sensation. It is usually somewhat ill- defined in extent but located in the epigastric region. It is a painless sensation and may be accompanied by a desire to vomit. The nauseous phase is often followed by vomiting, but not necessarily so. It may be accompanied by hypersalivation and an unpleasant taste sensation.
Nausea is accompanied by cessation of gastric phasic contractions and there is a simultaneous sustained contraction or spasm of the duodenum. The gastroduodenal motor patterns are probably only peripheral manifestations of a disturbance arising in the brain. Some causes of vomiting are:
Vomiting, or emesis, is the expulsion of the material in the stomach and upper intestinal tract through the mouth. It is a complex reflex action coordinated through the medulla. It is usually preceded by an increase in salivation, sweating and by an increased heart rate and feelings of nausea. These signs are characteristic of a general discharge of the autonomic nervous system. Emesis begins with a deep inhalation, closure of the glottis and elevation of the soft palate. The abdominal and thoracic muscles are contracted, raising the intraabdominal pressure, and this is transmitted to the stomach. The gastroesophageal sphincter relaxes and the increased abdominal pressure pushes the stomach contents into the esophagus. When the pressure is sufficiently great, the contents in the esophagus are forced through the hypopharyngeal sphincter to the mouth. Vomiting is accompanied by strong contractions of the upper part of the small intestine. This tends to force some of the contents of the intestine back into the stomach.
Input into the vomiting center (of the medulla) is from receptors throughout the body. The primary stimuli are tactile stimuli of the back of the throat, e.g., a finger thrust into the throat, gross distention of the stomach or duodenum increased pressure in the skull, rotating movements of the head producing dizziness, and excruciating pain. Some chemical agents, e.g., copper sulfate, also induce vomiting. Such chemicals act on chemoreceptors in the brain or parts of the G.I. tract. Too much vomiting can lead to excessive loss of fluid and salts from the body and can cause severe upset of the acid-base balance.
Food poisoning due to an infection or intoxication usually does not cause major pathological changes in the tissues. Those due to infections by Salmonella typhosa, causing typhoid fever, lead to a great increase in monocytes. There is particular involvement of the lymphatic tissue of the intestinal tract, principally Peyer's patches in the terminal ileum, which may lead to ulceration and necrosis. Erosion of adjacent blood vessels may cause intestinal hemorrhage. Lesions are usually confined to mucosa and submucosa, but may penetrate the other layers, leading to perforation. Healing of the intestinal lesions usually does not give rise to appreciable scarring or stricture formation.
Nonbacterial gastroenteritis is thought to be caused by viruses. It does not usually present any significant pathological changes.
Certain drugs which stimulate gastrointestinal peristalsis are used as cathartics. Physicians seldom prescribe these drugs, since the indications for their use are limited. More commonly, the health professional is faced with the problem of misuse of these drugs due to their easy accessibility in the form of over-the-counter preparations.
A cathartic is an agent which causes an increased elimination of fecal material from the bowel - three types are:
Drugs which harden the stools are referred to an antidiarrheal agents. These mainly act to decrease fecal transit time, allowing for a greater reabsorption of water, and thus hardening of the stools.