PATHPHYSIOLOGIC CONCEPTS OF GIT DISTURBANCES ANOREXIA Defined as

PATHPHYSIOLOGIC CONCEPTS OF GIT DISTURBANCES ANOREXIA Defined as a loss of appetite or desire for food, anorexia often occurs as a symptom with other GI alterations, including nausea, vomiting, and diarrhea. It can also be present with conditions not associated with the GIT, such as cancer.

• Anorexia nervosa is a condition in which one chooses not to eat because of a morbid fear of being fat. The term anorexia nervosa is actually a misnomer because of individuals who have this disorder still have a desire to eat and are still hungry, so by definition they are not truly anorectic.

NAUSEA • Nausea is a subjective unpleasant sensation that often precedes vomiting. Nausea is caused by distention or irritation anywhere in the GIT, but it can also be stimulated by higher brain centers. Interpretation of nausea occurs in the medulla which is either adjacent to or part of the vomiting center.

VOMITING • Vomiting is a complex reflex mediated through the vomiting center in the medulla oblongata of the brain. Afferent impulses originate in the stomach or duodenum in response to excessive distention or irritation, or sometimes they originate in response to chemical stimulation by emetics (agents that cause vomiting). Hypoxia and pain can also stimulate vomiting by means of activation of the vomiting center.

VOMITING • Vomiting can also occur through direct stimulation of an area of the brain adjacent to the vomiting center, called the chemoreceptor trigger zone, which lies in the brain stem. Activation of the chemoreceptor trigger zone can cause vomiting either directly or indirectly by its subsequent activation of the vomiting center

VOMITING • Input from higher brain centers in the cortex and increased intracranial pressure (ICP) can also stimulate vomiting , probably by directly stimulating center the vomiting center. Projectile vomiting occurs when the vomiting center is directly stimulated, frequently by increased ICP.

VOMITING • When the vomiting reflex is initiated in the vomiting center, it is carried out by activation of several cranial nerves to the face and throat, and spinal motor neurons to the diaphragm and abdominal muscles. Excitation of these pathways results in the coordinated response of vomiting. Certain symptoms generally precede vomiting, including nausea, tachycardia, and sweating.

DIARRHEA • Diarrhea is an increase in fluidity and frequency of stools. It may be large or small volume and may or may not contain blood. Large –volume diarrhea can occur as a result of the presence of a non-absorbable solute in the stool, called osmotic diarrhea, or as a result of irritation of the intestinal tract. The most common cause of large volume diarrhea due to irritation is a viral or bacterial infection of a large intestine or the distal small intestine.

DIARRHEA • Irritation of the intestines by a pathogen affects the mucosal layer, leading to increased secretory products, including to mucus. Micobial irritation also affects the muscular layer , leading to increased motility, Increased motility causes large amounts of water and electrolytes to be lost in the stool because the time available for their reabsorption in the colon is reduced. An individual who has sever diarrhea can die from hypovolemic shock and electrolyte irregularities. Cholera toxin released from the cholera bacteria is an example of a substance that strongly stimulates motility and directly causes secretion of water and electrolytes into the large intestine.

DIARRHEA • Small –volume diarrhea is characterized by frequent loss of small amounts of stool. Causes of this type of diarrhea include ulcerative colitis and Crohn’s disease. Both of these illnesses have physical and psychogenic components

CONSTIPATION • Constipation is defined as difficult or infrequent defication. Because frequency of stool varies among individuals, the second half of this definition is subjective and should be interpreted as a relative decrease in the number of stools for that particular individual. In general, bowel movements fewer than once every 3 days are considered to indicate constipation. Defecation can become difficult if the stool is hard and compact

CONSTIPATION • This can occur when an individual is dehydrated or if a bowel movement is delayed, which allows more water to be absorbed out of the stool as it sites in the large intestine. Bulk or high fiber diets keep stools moist by osmotically drawing water into the stool and by stimulating peristalsis of the colon by distention. Exercise promotes defecation by physical stimulation of the GIT. Therefore, individuals who lead sedentary lives are at higher risk of suffering from constipation

CONSTIPATION • . Sympathetic stimulation of the GIT decreases motility and can slow defecation. Sympathetc activity is increased in individuals who have long term stress. Certain drugs such as antacids and opiates also may cause constipation • Spinal cord trauma, intestinal neoplasm, and hypothyroidism can result in constipation.

GASTROESOPHAGIAL REFLUX DISEASE(GERD): • The condition of GERD is caused by the reflux of stomach contents into the esophagus. GERD is commonly called heartburn because of the pain that occurs when the acid normally present only in the stomach, enters and burns or irritates the esophagus. • Risk factors for GERD include male gender, increased body mass index(BMI), smoking, and regular alcohol intake.

CAUSES OF GERD • GERD usually occurs after a meal and results from conditions that either weaken the tone of the esophageal sphincter or increase the pressure in the stomach compared with the esophagus. By either of these mechanisms, acidic stomach contents move into the esophagus.

CAUSES OF GERD • The contents of the stomach are usually prevented from entering the esophagus by the esophageal sphincter. This sphincter normally opens only when a peristaltic wave delivering a bolus of food moves down the esophagus. When this happens, the smooth muscle of the sphincter relaxes, and food enters the stomach. It is important that the esophageal sphincter always remains closed except at this time, because many organs are crowded together in the abdominal cavity, causing abdominal pressure to be greater than thoracic pressure.

CAUSES OF GERD • Therefore, the tendency is for contents of the stomach to be pushed up into the esophagus. If one has a weakened or incompetent sphincter, it will not remain closed to stomach contents. Reflux will occur from the high pressure zone (the stomach)to the low pressure zone(the esophagus). A weakened sphincter can be a congenital defect or a result of damage to the esophagus. Repeated episodes of GERD may themselves worsen the condition by causing inflammation and scarring in the lower esophageal area.

CAUSES OF GERD • In some circumstances, even if the sphincter has normal tone, reflux will occur if there is an unusually high pressure gradient at the sphincter. For example, if stomach contents are excessive, abdominal pressure may increase significantly. This may result from an extra large meal, pregnancy, or obesity. High abdominal pressures tend to push the esophageal sphincter into the thoracic cavity, this exaggerates the pressure gradient between the esophagus and the abdominal cavity. Lying down, especially after a large meal, also contributes to reflux. • Reflux of stomach contents irritates the esophagus because of the high acid content in the stomach. Although the esophagus also has mucus producing cells, they are not as active or as prevalent as they are in the stomach.

CLINICAL MANIFESTATIONS • -Burning pain in the epigastric area, and may radiate to shoulders, back, or neck. • -Sour taste may accompany the pain. • -Pain usually occurs within 30 -60 minutes after a meal or during sleep, when the individual is lying down.

DIAGNOSTIC TOOLS • -A good history identifies many individuals at risk of GERD. • -A p. H probe passed into the lower esophageal area may reveal an abnormally low p. H (below 4. 0)in individuals who have GERD. • -Barium swallows.

COMPLICATIONS • -Vomiting and dysphasia with eating may occur. • -Chronic irritation of the esophagus can cause chronic inflammation, spasm of the muscles, and scarring of the esophagus, all of which may lead to stricture development, thereby interfering with or blocking food passage. • -Esophagus is an irritation of the lining of the esophagus characterized by cell changes that can result from chronic reflux. It is a premalignant condition that may lead to esophageal carcinoma.

TREATMENT • -Abdominal pressure can be reduced by eating more frequent small meals rather than large meals. If obesity is a problem, nutritional and exercise counseling are advised. • Sitting up during and after eating, and sleeping with the head elevated will reduce abdominal pressure on the esophageal sphincter. • Drinking extra fluids will help wash refluxed material out of the esophagus. • -Anti-reflux surgery may be considered if symptoms are resistant to treatment. • -Antacids may be used to neutralize the acidic content of the stomach

PEPTIC ULCER • The term of peptic ulcer refers to an erosion of the mucosal layer anywhere in the GIT, however, it usually refers to erosions in the stomach or duodenum. Gastric ulcer refers only to an ulcer in the stomach.

CAUSES OF PEPTIC ULCER • There are two main causes of ulcers: • -Too little mucus production or • -Too much acid being produced in the stomach or delivered to the intestine. • Decreased mucus production as a cause of ulcer: • Ulcers most commonly develop when the mucosal cells of the gut do not produce adequate mucus to protect against acid digestion.

CAUSES OF PEPTIC ULCER • Causes of decreased mucus production can include anything that decreases blood flow to the gut, causing hypoxia of the mucosal layer and injury to or death of mucus-producing cells. This type of ulcer is called ischemic ulcer. A particular type of ischemic ulcer that develops after a sever burn is called a Curling ulcer.

CAUSES OF PEPTIC ULCER • Decreased mucus production in the duodenum also can occur as a result of inhibition of mucus –producing glands, called Brunner’s glands, located there. Their activity is inhibited by sympathetic stimulation that is increased by chronic stress, thus making a connection between chronic stress and ulcer development • The main cause of decreased mucus production is related to infection with the bacterium Helicobacter pylori colonizes the mucus –secreting cells of the stomach and duodeneum, reducing their ability to produce mucus, Approximately 90% of duodenal ulcer and 70% of gastric ulcer show H. pylori infection.

CAUSES OF PEPTIC ULCER • The use of various drugs especially non steroidal anti inflammatory drugs(NSAIDs), is also associated with an increased risk of ulcer development. Aspirin, causes irritation of the mucosal wall, as do the other NSAIDs and glococorticosteroids. These grugs contribute to ulcer development by inhibiting protective PGs both systemically and in the gut wall.

CAUSES OF PEPTIC ULCER Approximately 10%of patients taking NSAIDs develop an active ulcer while a much higher percentage develops less serious erosions. Other drugs or foods associated with ulcer development include caffeine, alcohol, and nicotine. These drugs seem to injure the protective mucosal layer also.

EXCESS ACID AS A CAUSE OF ULCER • Acid production in the stomach is necessary for activation of stomach digestive enzymes. HCl is produced by the parietal cell in response to certain foods, drugs, hormones (as gastrin)histamine, and parasympathetic stimulation. Foods and drugs such as caffeine and alcohol stimulate the parietal cells to produce acid. Because gastrin stimulates the production of acid , anything that increases the secretion of gastrin can lead to excess acid

EXCESS ACID AS A CAUSE OF ULCER • The main example of this condition is called Zollinger-Ellison syndrome, a disease characterized by tumors of gastrin-secreting endocrine cells. Other causes of excess acid include excessive vagal stimulation to the parietal cells that is seen after severe brain injury or trauma. Ulcers that develop under these circumstances are called Cushing ulcers. Excess vagal stimulation during psychological stress may also cause excess HCl production.

CLINICAL MANIFESTATIONS • -Burning abdominal pain often occurs at night. The pain is usually located in the midline epigastric area, and is often rhythmic in nature. • -Pain that occur when the stomach is empty, often signifies a duodenal ulcer. • -Pain that occurs immediately after or during eating suggest a gastric ulcer, occasionally, the pain may be referred to the back or shoulder. • -The occurrence of pain often comes and goes, it sometimes occurs daily for several weeks and then disappears. • -Weight loss is common with gastric ulcers, weight gain may occur with duodenal ulcers because eating relieves the discomfort.

DIAGNOSTIC TOOLS • -Ulcers are diagnosed primarily by history and endoscopy and tissue samples can also be taken for biopsy and the presence or absence of H, pylori can be determined. • -H. pylori infection may also be diagnosed by blood tests for antibody.

COMPLICATIONS • -An ulcer may in some instances go through all mucosal layers, causing perforation of the gut. Because gut contents are not sterile, this can lead to infection of the abdominal cavity. • -Obstruction of the lumen of the GIT may occur as a result of repeated episodes of injury, inflammation and scarring. Obstruction most often at the pylorus, the narrow passageway between the stomach and the small intestine. Obstruction causes feeling of stomach and epigastric distention, nausea and vomiting. • -Hemorrhage may occur when the ulcer has eroded an artery or vein in the gut. This can result in hematomesis(vomiting of blood)or in melena (passage of upper GI blood in the stool)

TREATMENT • -Educate patients that avoidance of alcohole and caffeine improves symptoms and increases healing of a pre-existing ulcer. • -Discontinue or reduce NSAID ingestion, • -Prescribe antihistamines. • -Stress management , relaxation techniques, or sedatives can be used to relieve psychological influences.

MALABSORPTION • Failure of the small intestine to absorb certain foodstuffs is called malabsorption. Inability to absorb can be (1)of one type of amino acid, fat, sugar, or vitamin, (2)of all amino acids, fats, sugar, or (3)of all fat-soluble vitamins. Malabsorption of everything absorbed in one segment of the small intestine can occure, with other small –intestine segment being spared.

MALABSORPTION • Causes of malabsorption include pancreatic digestive enzyme deficiency, microorganism infection, damage to the mucosal layer of the gut, or, for fats and fat-soluble vitamins, impairment of bile production or lymph function. Lactose malabsorption can result from the inability to break down lactose into absorbable monosaccharides. Lactose malabsorption can result from a congenital deficiency in the enzyme lactase or a decrease in lactase after an intestinal disease, a disease characterized by injury to the villi that apparently is caused by a hypersensitivity to gluten, product of wheat.

MALABSORPTION CLINICAL MANIFESTATIONS • Generalized symptoms usually include those related to GIT or to the loss of fat soluble vitamins: • -Fat malabsorption results in steatorrhea (fat in the stool). Diarrhea, flatulence, and cramps often occur. Stools are bulky but of light weigh, float, and are malodorous. • -Bile salt deficiency results in malabsorption of fat-soluble vitamins, causing the following:

MALABSORPTION CLINICAL MANIFESTATIONS • -Vitamin A deficiency-night blindness. • -Vitamin D deficiency-bone demineralization and increased risk of fractures. • -Vitamin K deficiency –poor coagulation with prolonged prothrombin time, • Easy petechia (hemorrhagic spots on the skin) • -Vitamin E deficiency –perhaps resulting in poor immune function. • -Lactose malabsorption results in osmotic diarrhea and flatulence.

MALABSORPTION Diagnostic Tools • -The presence of over 7 g of fat per day in the stool of an adult is considered malabsorption. • -Weight loss or failure to gain weight in infancy or young childhood may indicate malabsorption • COMPLICATIONS • -Failure to growing may occur in severe cases, leading to malnutrition, infection, and even death.

MALABSORPTION TREATMENT • -Identification of the cause of malabsorption. • -Provision of needed nutrients through other food sources or supplements. •