| PHASES OF GI CONTROL | (1) Cephalic:
receptors in the head are stimulated by sight, smell, taste and chewing.
These activate parasympathetic and sympathetic nerves that go into the
abdomen and activate the GI tract nerve plexuses of Fig 17-13 to stimulate
secretion of digestive chemicals and smooth muscle contraction of the GI
tract walls.
(2) Gastric: Distension and chemical changes in the stomach cause secretion of digestive chemicals in the stomach using the short and long reflexes of Fig 17-13. This phase is controlled by short and long reflexes and by gastrin. (3) Intestinal: Distension and chemical changes in the intestinal tracts cause secretion of digestive chemicals and movement of the smooth muscle walls using the short and long reflexes of Fig 17-13. This phase is mediated by short and long reflexes, CCK and a few other hormones. (Know CCK). |
| GI TRACT REGULATION BY ANATOMIC LOCATION, TOP TO BOTTOM | |
| MOUTH, PHARYNX, ESOPHAGUS
17-14, 17-15 |
Phases:
(1) Chewing and secretion of saliva. (2) Swallowing which requires closing of the glottis, then the epiglottis over the trachea. (3) Esophageal phase: relaxing of the upper sphincter, movement of food by peristaltic waves (waves of smooth muscle contraction) and opening of the lower esophageal sphincter. |
| STOMACH
17-16, 17-17
17-17, 17-18, 17-20
17-21
17-19, do not need to know.
17-21
|
(1) Gastrin:Increased
peptide concentration and lower H+ in the stomach stimulate gastrin release.
When food enters the stomach it acts as a buffer, lowering H+, stimulating
gastrin release from cells in the stomach wall. Gastrin stimulates HCl
(gastric acid) release in the stomach. When chyme enters the duodenum
its high acidity inhibits gastrin secretion.
(2) HCl: Release from the parietal cells (Fig 17-17) is caused by gastrin and by nerve stimulation during the cephalic phase on in parietal cell receptors. The H,K-ATPase pumps in these cells are then mobilized to pump out H+ (Fig 17-18). (3) Pepsin: Input from nerve plexuses stimulated during the cephalic and gastric phases stimulate release of pepsinogen from chief cells in the stomach wall. In the lumen pepsinogen is converted to the active enzyme pepsin by the high H+. Pepsin can then digest protein. (Fig 17-21). The chief cells do not contain active pepsin because then pepsin would digest its own cell from the inside. In general, the inactive digestive enzymes inside a cell are called zymogens. They are activated when they are released into the lumen. |
| HOW THE STOMACH FILLS
AND EMPTIES
17-22, 17-23 17-24, do not need to know. |
The smooth muscles
of the stomach relax by parasympathetic reflexes to allow it fill
with as much as 1.5 liters of food.
The stomach has pacemaker cells in the smooth muscle that fire about 3 times per minute. These depolarizations are too small to contract the smooth muscle unless the smooth muscle is depolarized by neurotransmitters and hormones that are released in response to food. The depolarizations then cause the smooth muscle to contract. This causes peristaltic waves which push chyme into the small intestine a little at a time through the pyloric sphincter. |
| PANCREATIC SECRETIONS
17-25, 26, 27, 28. Know Table 17-5 17-28 |
Pancreatic enzymes:
(1) Trypsin and chymotrypsin digest proteins (2) Lipase digests fats (3) Amylase digests carbohydrates Their release is stimulated by CCK from the small intestine. Taste of food can also release these enzymes. Bicarbonate from the pancreas neutralizes the H+ that comes in from the stomach. |
| BILE SECRETIONS
17-29, 30, 31 17-30
|
Fatty acids in the
small intestine stimulates CCK secretion, which stimulates gallbladder
contraction and release of bile into the small intestine.
Bile contains several chemicals. For digestion the most important are bile salts, synthesized in the liver.They are reabsorbed into the ileum of the small intestine and taken back to the liver by veins to be reused. Bile pigments are derived from heme that
comes from red blood cells broken down in spleen and liver. Bile pigments
give urine its yellow color.
Cholesterol is also found in bile. The liver makes cholesterol and can get rid of some of the bile if there is too much in the body. The liver cells are called hepatocytes. They make bile salts and cholesterol. Liver cells do much more that is beyond the scope of this chapter (Table 17-1). |
| SMALL INTESTINE | The small intestine is about 1.5 inches in diameter and 9 feet long. It is divided into duodenum, jejunum and ileum. Water goes into its lumen from plasma, glands and drinking. The intestinal epithelium secretes mineral ions into the lumen and water follows these by osmosis. |
| Motility
17-32 |
Pacemaker cells
in the longitudinal smooth muscle cause smooth muscle contraction that
mixes up the chyme and brings it to the epithelium where the nutrient molecules
are absorbed. The movement is called segmentation and mixes up chyme rather
than propel it forward. Nerve and hormone input can increase the intensity
of segmentation contraction.
After most of a meal has been absorbed the segmentation is replaced by the migrating motility complex which moves undigested material into the large intestine. |
| LARGE INTESTINE
17-33 |
The large intestine is about 2.5 inches in diameter and 4 feet long. The first portion is the cecum, followed by the ascending, transverse and descending colon which ends in the rectum. |
| Ileocecal sphincter | Chyme enters from the small intestine through this sphincter into the large intestine. It is usually closed, but when the small intestine near it contracts it relaxes to let chyme in. |
| Absorption | About 1500 ml of chyme enters the colon daily, mainly from secretions in the lower small intestine, not so much from food. The colon mucosa lacks villi and it absorbs only about 4% of what is absorbed in the whole GI tract. |
| Sodium and potassium | Sodium is actively transported from the colon into the blood. Potassium is moved into the colon. Infections which cause diarrhea can cause a severe depletion of potassium. |
| Bacterial fermentation | Bacteria digest polysaccharide that the body cannot. This produces gases containing mainly nitrogen and CO2. This produces 400-700 ml/day gas or flatus. |
| Motility and defecation | Contents stay in the colon 18-24 hours. 3-4 times a day, usually following a meal, contraction of the colon smooth muscle wall, called mass movement, moves the contents toward the rectum. The internal anal sphincter and later the external anal sphincter (which is under voluntary control) relax by reflex responses to allow defecation. Feces contains about 100 grams of water and 50 grams of solid. The solids are mainly bacteria, undigested polysaccharide, bile pigments, cholesterol and some electrolytes, mainly potassium. |
| PATHOPHYSIOLOGY OF THE GI TRACT | |
| Ulcers | The acid and pepsin
in the stomach usually do not digest the stomach wall, which is protected
by
(1) alkaline mucus, (2) tight junctions and (3) continual replacement of the cells. In ulcers the protective mucosal barrier breaks down. The major factor may be a helicobacter bacteria. Antibiotics kill the bacteria and heal ulcers. HCl acid secretin can aggravate ulcers so drugs to inhibit acid secretion help. |
| Vomiting | Vomiting the contents of the stomach and upper small intestine is a complex reflex coordinated in the vomiting center of the brain stem. Neural input to the vomiting center from stretch receptors and chemoreceptors in the intestinal wall can initiate vomiting. Vomiting to void toxic substances is useful. The utility of vomiting in such disorders as motion sickness is less clear. In vomiting there are strong abdominal muscle contractions, increasing abdominal pressure, and the lower esophageal sphincter relaxes. This forces the contents up and out, including H+ ions. Excessive vomiting can lower body acidity to too low a value. |
| Gallstones | Bile contains bile
salts, cholesterol and phospholipids. The most common cause of gallstones
is too much cholesterol in the bile, which crystallizes. Women have
gallstones about twice as often as men.
Blocking the common bile duct with gallstones can result in severe digestive problems. See Fig 17-4 to see why. |
| Lactose intolerance | Lactose is milk sugar, a disaccharide (glucose and galactose). It is digested by lactase into monosaccharides (one-ring sugars). In people of Northern European descent, lactase levels decrease in childhood. The undigested lactose moves into the colon, where bacteria digest it, producing diarrhea and gas. |
| Diarrhea | Results from increased fluid secretion or decreased fluid absorption or both. Certain bacteria, protozoa and viruses can disrupt the epithelium of the colon, altering ion transport processes, resulting in more water in the colon and diarrhea. Dehydration and severe potassium depletion can occur. |
| GOOD LUCK! |