Introduction:The digestive system contributes to homeostasis by breaking down food into forms that can be absorbed and used

by body cells. It also absorbs water, vitamins, and minerals, and eliminates wastes from the body. The literal meaning of Digestion (Dis- apart; gerere _ to carry). The organs involved in the breakdown of foodcollectively called the digestive system.

ANATOMY AND PHYSIOLOGY OF COLON.

The small intestine (small in diameter compared to the large intestine) is divided into three sections,

The duodenum, about 25 cm (10 in) long, receives chyme from the stomach through the pyloric sphincter. Ducts that empty into the duodenum deliver pancreatic juice and bile from the pancreas and liver, respectively. The jejunum, about 2.5 m (8 ft) long, is the middle section of the small intestine. The ileum, about 3.6 m (12 ft) long, is the last section of the small intestine. It ends with the ileocecal valve (sphincter), which regulates the movement of chyme into the large intestine and prevents backward movement of material from the large intestine.

The functions of the small intestine include

Mechanical digestion. Segmentation mixes the chyme with enzymes from the small intestine and pancreas. Bile from the liver separates fat into smaller fat globules. Peristalsis moves the chyme through the small intestine. Chemical digestion. Enzymes from the small intestine and pancreas break down all four groups of molecules found in food (polysaccharides, proteins, fats, and nucleic acids) into their component molecules. Absorption. The small intestine is the primary location in the GI tract for absorption of nutrients:

Carbohydrates, proteins, nucleic acids, and water-soluble vitamins. The components of these molecules are absorbed by facilitated diffusion or active transport. They are then passed to blood capillaries. Vitamin B12. Vitamin B12 combines with intrinsic factor (produced in the stomach) and is absorbed by receptor-mediated endocytosis. It is then passed to the blood capillaries. Lipids and fat-soluble vitamins. Because fat-soluble vitamins and the components of lipids are insoluble in water, they are packaged and delivered to cells within water-soluble clusters of bile salts called micelles. They are then absorbed by simple diffusion and, once inside the cells, mix with cholesterol and protein to form chylomicrons. The chylomicrons are then passed to the lymphatic capillaries. When the lymph eventually empties into the blood, the chylomicrons are broken down by lipoprotein lipase, and the breakdown products, fatty acids and glycerol, pass through blood capillary walls to be absorbed by various cells. Water and electrolytes. About 90 percent of the water in chyme is absorbed, as well as various electrolytes (ions), including Na -, K-, Cl, nitrates, calcium, and iron.

Modifications of the mucosa for its various specialized functions in the small intestine include the following:

The plicae circulares (circular folds) are permanent ridges in the mucosa that encircle the inside of the small intestine. The ridges force the food to spiral forward. The spiral motion helps mix the chyme with the digestive juices. Villi (singular, villus) are fingerlike projection that cover the surface of the mucosa, giving it a velvety appearance. They increase the surface area over which absorption and digestion occur. The spaces between adjacent villi lead to deep cavities at the bases of the villi called intestinal crypts (crypts of Lieberkhn). Glands that empty into the cavities are called intestinal glands, and the secretions are collectively called intestinal juice. Microvilli are microscopic extensions of the outer surface of the absorptive cells that line each villus. Because of their brushlike appearance (microscopically), the microvilli facing the lumen form the brush border of the small intestine. Like the villi; the microvilli increase the surface area over which digestion and absorption take place.

The villi of the mucosa have the following characteristics:

An outer epithelial layer (facing the lumen) consists of the following cell types:

Absorptive cells, the primary cell type of the epithelial layer, synthesize digestive enzymes called brush border enzymes that become embedded in the plasma membranes around the microvilli. Various nutrients in the chyme that move over the microvilli are broken down by these brush border enzymes and subsequently absorbed. Goblet cells, located throughout the epithelial layer, secrete mucus that helps protect the epithelial layer from digestion. Enteroendocrine cells secrete hormones into blood vessels that penetrate the villus. Paneth cells, located in the epithelial layer facing the intestinal crypts, secrete lysozyme, an enzyme that destroys bacteria.

An inner core of lamina propria (connective tissues) contains blood capillaries and a small lymphatic capillary called a lacteal.

The submucosa that underlies the mucosa of the small intestine bears the following modifications:

Brunner's (duodenal) glands, found only in the submucosa of the duodenum, secrete an alkaline mucus that neutralizes the gastric acid in the incoming chyme. Peyer's patches (aggregated lymphatic nodules), found mostly in the submucosa of the ileum, are clusters of lymphatic nodules that provide a defensive barrier against bacteria

Disorders of small intestine can be divided on the basis of its parts. First part is duodenum and hence diseases of duodenum are- duodenal ulcers, duodenal atresia. Then the second part is jejunum and its most common disorder is celiac spure. The third part is ilieum and its disorders are inflammatory bowel disease and small bowel obstruction is one of the commonest disorder small intestine. So, let us see those diseases in detail. 1. Duodenal disorders:PEPTIC ULCERS In the digestive system, an ulcer is an area where tissue has been destroyed by gastric juices and stomach acid. Peptic ulcer disease is a general term for ulcers that occur in the stomach or duodenum (upper part of the small intestine). Incidence Peptic ulcers are a very common condition in INDIA and throughout the world.

In India, about 10% of the population will develop a duodenal ulcer at some point in their lives. Peptic ulcer disease affects about 4.6 million people annually. The occurrence of peptic ulcer disease is similar in men and women. Approximately 11%-14% of men and 8%-11% of women will develop peptic ulcer disease in their lifetime.

The mortality rate for peptic ulcer disease is approximately one death per 10,000 cases. The mortality rate due to ulcer hemorrhage is approximately 5%. Ulcers can occur at any age, although they are rare in children and teenagers. Peptic Ulcers Causes In the past it was throught that ulcers were caused by lifestyle factors such as eating habits, cigarette smoking, and stress.

Research done in the 1980s showed that ulcers are caused by infection with a bacterium named Helicobacter pylori, usually called H pylori. Aspirin, nonsteroidal anti-inflammatory drugs (such as ibuprofen and naproxen), and newer anti-inflammatory medications (such as celecoxib[Celebrex]) Alcohol Stress: physical (severe injuries or burns , major surgery) or emotional Caffeine Cigarette smoking Radiation therapy:-used for diseases such as cancer H pylori bacteria spread through the stools (feces) of an infected person.

A rare condition called Zollinger-Ellison syndrome causes peptic ulcers as well as tumors in the pancreas and duodenum.

Pathophysiology:-

Peptic Ulcer Symptoms Ulcers do not always cause symptoms. Sometimes, a serious complication such as bleeding is the first sign of an ulcer. The most common symptom of peptic ulcers is abdominal pain.

The pain is usually in the upper middle part of the abdomen, above the belly button (navel) and below the breastbone. The pain can feel like burning or gnawing, and it may go through to the back. Pain often comes several hours after a meal when the stomach is empty. The pain is often worse at night and early morning. It can last anywhere from a few minutes to several hours. The pain may be relieved by food, antacids, or vomiting. Other symptoms of peptic ulcers include the following:

Nausea Vomiting Loss of appetite Loss of weight

Severe ulcers may cause bleeding in the stomach or duodenum. Bleeding is sometimes the only symptom of an ulcer.

Vomiting of blood or dark material that looks something like coffee grounds: This is an emergency and warrants an immediate visit to an emergency department. Blood in the stool or black, tarry, sticky-looking stools Slow bleeding is often more difficult to detect, because it has no dramatic symptoms.

The usual result is low blood cell count (anemia). The symptoms of anemia are tiredness (fatigue), lack of energy (lethargy), weakness, rapid heartbeat (tachycardia), and pales skin (pallor). Peptic Ulcer Diagnosis To confirm that a person has an ulcer, he or she will most likely undergo a diagnostic imaging test. The two most widely used tests are:

Upper GI series (UGI): This is a type X-ray. The patient is given a chalky liquid to drink that increases the contrast on the X-ray, making certain features easier to see. Because this liquid contains barium, this test is sometimes called a barium swallow. Endoscopy (EGD): An endoscope is a thin, flexible tube with a tiny camera on the end. The patient is given a mild sedative, and then the tube is passed through the mouth into the stomach. Tiny samples of the tissue will be taken (biopsy), which are examined under a microscope. Three types of tests are available to detect H pylori.

Blood tests: These tests detect the bacteria by measuring antibodies to the bacteria. Antibodies are proteins produced by the immune system to defend against an "invader" such as H pylori. Breath test: This test detects H pylori by measuring carbon dioxide in the breath of a person who has drunk a special liquid. The body gets rid of this carbon by breathing it out as carbon dioxide. This test is more accurate than the blood test but is more difficult to carry out. Tissue tests: These tests are used only if an endoscopic biopsy has been done, because a sample of tissue from the stomach is needed to detect the bacteria.

Peptic Ulcer Medical Treatment The following treatments are recommended for ulcers:

Lifestyle changes: Quit smoking, avoid alcohol, aspirin, and NSAIDs Acid-blocking medications Medications that protect the lining of the stomach and duodenum "Triple-therapy" or "dual-therapy" regimens for ulcers caused by H pylori No single medication works to get rid of H pylori infection. Two combinations have been found that work well in most people.

Triple therapy: The combination of bismuth subsalicylate (for example, Pepto-Bismol) and the antibiotics tetracycline and metronidazole are effective in 80%-95% of people and is the current standard of therapy. The bismuth subsalicylate and tetracycline have to be taken 4 times a day and the metronidazole 3 times a day. Dual therapy: This therapy was developed as a response to the complexity and side effects of triple therapy. It comprises 2 antibiotics, amoxicillin and metronidazole, both taken as pills 3 times a day. o Clarithromycin can be substituted for the 15%-25% of people whose infections are resistant to metronidazole. o Sometimes an acid pump inhibitor such as omeprazole. Peptic Ulcer Surgery Medical therapy works in most people with peptic ulcers. Surgery is a good alternative to medical therapy for these people. Surgical operations often used in peptic ulcers include the following:

Vagotomy: Cutting the vagus nerve, which transmits messages from the brain to the stomach, can reduce acid secretion. However, this can also interfere with other functions of the stomach. A newer operation cuts only the part of the nerve that affects acid secretion. Antrectomy: This is often done in conjunction with a vagotomy. It involves removing the lower part of the stomach (the antrum). This part of the stomach produces a hormone that increases production of stomach acid. Adjacent parts of the stomach may also be removed. Pyloroplasty: This procedure also is sometimes done with vagotomy. It enlarges the opening between the stomach and duodenum (the pylorus) to encourage passage of partially digested food. Once the food has passed, acid production normally stops.

Tying off an artery: If bleeding is a problem, cutting off the blood supply (artery) to the ulcer can stop the bleeding. Nursing management Nursing Assessment 1. Assess for chronic use of certain medications (such as aspirin, steroids). 2. Collect information of complaints that brought client to the hospital. 3. Obtain history of onset and progression of symptoms. 4. Obtain information of diet, use of alcohol and tobacco, ingestion of irritating foods, previous diseases or infections of GI tract, emotional stress. 5. Assess connection of pain attacks to meals, certain drugs, ingestion of coffee, alcohol. 6. Perform complete physical assessment including weight, vital signs, signs of GI bleeding, and acute abdomen. 7. Assess diagnostic tests and procedures for abnormal values. Nursing Diagnosis 1. Increased risk of GI bleeding and perforation of stomach, related to gastric or intestinal wall erosion. 2. Increased risk of pyloric obstruction as complication of the peptic ulcer. 3. Increased risk of anemia due to acute or chronic GI bleeding, related to ulcer. 4. Pain and heartburn, related to diagnosis of peptic ulcer. 5. Appetite changes and weight changes due to symptoms of the ulcer. 6. Increased risk of aspiration due to vomiting, related to ulcer. 7. Anxiety related to the symptoms of disease and fear of the unknown. Interventions 1. Assess, report , and record signs and symptoms and reactions to treatment. 2. Monitor fluids input and output closely. 3. Administer antacid agents, analgesics, H2-receptors antagonists, anticholinergics, sedatives as prescribed, monitor for side effects. 4. Monitor clients vital signs and signs of possible GI bleeding or perforation closely. 5. Monitor laboratory tests results (CBC, electrolytes, Hb levels) for abnormal values. 6. Undertake appropriate intervention in case of GI bleeding, vomiting, or perforation.

7. Provide prescribed diet avoid irritating foods, coffee, etc. 8. Prepare client and his family for surgical intervention if required for recurrent ulcer, hemorrhage, or perforation. 9. For client after surgical intervention provide postoperative care and inform about possible postoperative complications, such as dumping syndrome. 10. Provide emotional support to client, explain all procedures to decrease anxiety and to obtain cooperation. 11. Instruct client regarding disease progress, diagnostic procedures, treatment and its complications, home care, daily activities, diet, restrictions and follow-up. Complications

Gastrointestinal bleeding. Perforation Penetration is when the ulcer continues into adjacent organs such as the liver and pancreas. Scarring and swelling due to ulcers causes narrowing in the duodenum and gastric outlet obstruction. Patient often presents with severe vomiting.

2. DUODENAL ATRESIA
Definition Duodenal atresia is a condition in which the first part of the small bowel (the duodenum) has not developed properly. It is not open and cannot allow the passage of stomach contents. Incidence Duodenal atresia is seen in more than 1 in 10,000 live births. Approximately 2030% of infants with duodenal atresia have Down syndrome. Duodenal atresia is often associated with other birth defects.

Causes The cause of duodenal atresia is unknown, but it is thought to result from problems during an embryo's development in which the duodenum does not normally change from a solid to a tube-like structure.

Pathophysiology Duodenal maldevelopment occurs secondary to either inadequate endodermal proliferation (gut elongation outpaces proliferation) or failure of the epithelial solid cord to recanalize (failure of vacuolization). Multiple investigators have demonstrated that the epithelium of the duodenum proliferates during 30-60 days' gestation, completely plugging the duodenal lumen. A subsequent process termed vacuolation occurs whereby the solid duodenum is recanalized. Vacuolation is believed to occur by way of apoptosis, or programmed cell death, which occurs during normal development within the lumen of the duodenum. Occasionally, duodenal atresia is associated with annular pancreaspancreatic tissue that surrounds the entire circumference of the duodenum. This is likely due to failure of duodenal development rather than robust and/or abnormal growth of the pancreatic buds. At the cellular level, the GI tract develops from the embryonic gut, which is composed of an epithelium derived from endoderm, surrounded by cells of mesodermal origin. Cell signaling between these two embryonic layers appears to play a critical role in coordinating patterning and organogenesis of the duodenum. Sonic hedgehog genes encode members of the Hedgehog family of cell signals. Both are expressed in gut endoderm, whereas target genes are expressed in discrete layers in the mesoderm. Mice with genetically altered sonic hedgehog signaling display duodenal stenosis, which suggests that genetic defects in the sonic hedgehog family of genes may influence the development of duodenal abnormalities.

Symptoms

Upper abdominal swelling may or may not be present Early vomiting of large amounts, which may be greenish (containing bile) Continued vomiting even when infant has not been fed for several hours Absent urination after first few voidings Absent bowel movements after first few meconium stools

Diagnostic evaluation A fetal ultrasound may show excessive amounts of amniotic fluid in the womb, a condition called polyhydramnios. It may also show swelling of the baby's stomach and part of the duodenum. An abdominal x-ray may show air in the stomach and first part of duodenum, with no air beyond that. This is known as the double-bubble sign.

Treatment Medical management is always symptomatic. A tube is placed to decompress the stomach. Dehydration and electrolyte abnormalities are corrected by providing fluids through an intravenous tube. An evaluation for other congenital anomalies should be performed.

Surgical Therapy Duodenal atresia and stenosis are treated surgically. In patients with duodenal obstruction, a duodenoduodenostomy is the most commonly performed procedure. But duodenojejunostomy is now uncommonly performed due to its higher risk of long-term complications. Duodenal repair may be performed via a right upper quadrant incision, an umbilical incision, or laparoscopically, depending on surgeon preference. Prognosis Recovery from the duodenal atresia is expected after treatment. Untreated, the condition is deadly. Complications

Other birth defects Dehydration

After surgery, there may be late complications such as:

Swelling of the first part of the small bowel (megaduodenum) Problems with movement through the intestines Gastroesophageal reflux. Nursing management.

1. Assess, report , and record signs and symptoms and reactions to treatment. 2. Monitor fluids input and output closely. 3. Monitor clients vital signs and sign. 4. Monitor laboratory tests results (CBC, electrolytes, Hb levels) for abnormal values. 5. Undertake appropriate intervention in case of GI bleeding, vomiting, or perforation. 6. Prepare client and his family for surgical intervention.

JEJUNUM DISORDERS.
Celiac disease / Celiac spure Celiac sprue, also known as celiac disease, gluten-sensitive enteropathy, and gluten-induced enteropathy, is a chronic disease of the digestive tract that interferes with the digestion and absorption of nutrients from food. As a result, celiac sprue is often considered a malabsorption disorder. Celiac Sprue Causes Celiac sprue results from a combination of immunological responses to an environmental factor (gluten) and genetic factors. People need both a genetic predisposition and the exposure to gluten in order to develop celiac sprue.
o

Immune mechanisms The interaction of gliadin (a specific gluten present in certain grain products) with the lining of the small intestine is critical in the development of celiac sprue. When people with celiac sprue eat foods containing gluten, gliadin is identified by the immune system as a threat. As a result, the body produces antibodies called antigliadin antibodies. Antigliadin antibodies are directed against gliadin. The presence of these autoantibodies suggests that autoimmunity plays a role in the disease process of celiac sprue.

Genetic factors: Genes play an important role in celiac sprue. Celiac disease occurs much more frequently in relatives of persons with celiac sprue than in the general population.

Pathophysiology:

Celiac Sprue Signs and Symptoms Ages 3 to 9 months

Acutely ill; severe diarrhea and vomiting Irritability Possible failure to thrive

Ages 9 to 18 months

Slackening of weight followed by weight loss Abnormal stools Pale, soft, bulky Offensive odor Greasy (steatorrhea) May increase in number Abdominal distention Anorexia, discoloration of teeth Muscle wasting: most obvious in buttocks and proximal parts of extremities Hypotonia, seizures Mood changes: ill humor, irritability, temper tantrums, shyness Mild clubbing of fingers Vomiting: usually occurs in the evening Aphthous ulcers, dermatitis

Older Child and Adult

Signs and symptoms are commonly related to nutritional or secondary deficiencies resulting from disease. Anemia, vitamin deficiency (A, D, E, K) Hypoproteinemia with edema Hypocalcemia, hypokalemia, hypomagnesemia Hypoprothrombinemia from vitamin K deficiency Disaccharide (sugar) intolerance Osteoporosis due to calcium deficiency Anorexia, fatigue, weight loss. May have colicky abdominal pain, distention, flatulence, constipation, and steatorrhea.

Diagnostic Evaluation:

Small bowel biopsy, which demonstrates characteristic abnormal mucosa. Hemoglobin, folic acid, and Vitamin K levels may be reduced. Prothrombin time may be prolonged. Elevated immunoglobulin (Ig) A endomysium antibodies and IgA anti-tissue transglutaminase antibodies. Total protein and albumin may be decreased. 72 hour stool collection for fecal fat is increased.

D-xylose absorption test decreased blood and urine levels. Sweat test and pancreatic function studies may be done to rule out cystic fibrosis in child.

Therapeutic Interventions:

Dietary modifications includes a lifelong gluten-free diet, avoiding all foods containing wheat, rye, barley, and possibly, oats. In some cases, fats maybe reduced. Lactose and sucrose may be eliminated from diet for 6 to 8 weeks, based on reduced disaccharidase activity.

Nursing Interventions:

Monitor dietary intake, fluid intake and output, weight, serum electrolytes, and hydration status. Make sure that the diet is free from causative agent, but inclusive of essential nutrients, such as protein, fats, vitamins, and minerals. Maintain NPO status during initial treatment of celiac crisis or during diagnostic testing. Provide parenteral nutrition as prescribed. Provide meticulous skin care after each loose stool and apply lubricant to prevent skin breakdown. Encourage small frequent meals, but do not force eating if the child has anorexia. Use meticulous hand washing technique and other procedures to prevent transmission of infection. Assess for fever, cough, irritability, or other signs of infection. Teach the parents to develop awareness of the childs condition and behavior; recognize changes and care for child accordingly. Stress that the disorder is lifelong; however, changes in the mucosal lining of the intestine and in general clinical conditions are reversible when dietary gluten is avoided.

3. ILIEUM

DISORDERS.

Inflamatory bowel disease.

In medicine, inflammatory bowel disease (IBD) is a group of inflammatory conditions of the colon and small intestine. The major types of IBD are Crohn's disease and ulcerative colitis. Causes IBD is called an idiopathic disease (disease with an unknown cause). An unknown factor/agent (or a combination of factors) triggers the bodys immune system to produce an inflammatory reaction in the intestinal tract that continues without control. As a result of the inflammatory reaction, the intestinal wall is damaged leading to bloody diarrhea and abdominal pain. Genetic, infectious, immunologic, and psychological factors have all been implicated in influencing the development of IBD. There is a genetic predisposition (or perhaps susceptibility) to the development of IBD. However, the triggering factor for activation of the bodys immune system has yet to be identified. Factors that can turn on the bodys immune system include an infectious agent (as yet unidentified), an immune response to an antigen (eg, protein from cow milk), or anautoimmune process. As the intestines are always exposed to things that can cause immune reactions, more recent thinking is that there is a failure of the body to turn off normal immune responses. Inflammatory Bowel Disease Symptoms Symptoms may range from mild to severe and generally depend upon the part of the intestinal tract involved. They include the following:

Abdominal cramps and pain Bloody diarrhea Severe urgency to have a bowel movement Fever , Loss of appetite Weight loss, Anemia (due to blood loss)

Signs and symptoms

Crohn's disease Defecation Tenesmus Fever Fistulae Weight loss Often porridge-like, sometimes steatorrhea Less common Common Common Often

Ulcerative colitis Often mucus-like and with blood More common Indicates severe disease Seldom More seldom

Diagnostic evaluation Stool examination

A stool examination is done to eliminate the possibility of bacterial, viral, or parasitic causes of diarrhea. A fecal occult blood test is used to examine stool for traces of blood that cannot be seen with the naked eye. Complete blood count An increase in the white blood cellcount suggests the presence of inflammation in the body.

If you have severe bleeding, the red blood cell count may decrease and hemoglobinlevel may fall (anemia). Both the above tests are not diagnostic of IBD, as they may be abnormal in many other diseases. Barium x-ray

Upper gastrointestinal (GI) tract: This exam uses x-rays to find abnormalities in the upper GI tract (esophagus, stomach,duodenum, sometimes the small

intestine). For this test, you are required to swallow barium (a chalky white substance). When barium is swallowed, it coats the inside of the intestinal tract, which can be documented on x-rays. If you have Crohn's disease, abnormalities will be seen on barium x-rays.

Lower gastrointestinal (GI) tract: In this exam, barium is given in an enema that is retained in the colon while x-rays are taken. Abnormalities will be noted in the rectum and colon in persons with Crohn's disease and ulcerative colitis. Sigmoidoscopy Colonoscopy A colonoscopy is an examination similar to a sigmoidoscopy, but with this procedure, the entire colon can be examined. Upper endoscopy: If you have upper GI symptoms (nausea, vomiting), anendoscope (narrow, flexible tube with a light source) is used to examine the esophagus, stomach, and the duodenum. The endoscope is inserted through the mouth, and the stomach and duodenum are examined for ulceration. Ulceration occurs in the stomach and duodenum in 5-10% of persons with Crohn's disease. Medications These include aminosalicylates, corticosteroids, immune modifiers, antitumornecrosis factor (TNF) agents, and antibiotics.

Aminosalicylates are aspirin like anti-inflammatory drugs. There are 5 aminosalicylate preparations available for use : sulfasalazine (Azulfidine),mesalamine (Asacol, Pentasa), olsalazine(Dipentum), and balsalazide (Colazal). These drugs can be given either orally or rectally (enema, suppository formulations). Corticosteroids

Corticosteroids may be administered by a variety of routes, depending upon the location and severity of disease; they may be administered intravenously (methylprednisolone, hydrocortisone), orally (prednisone, prednisolone, budesonide, dexamethasone), or rectally (enema, suppository, foam preparations). Immune modifiers

Immune modifiers include 6-mercaptopurine (6-MP, Purinethol) andazathioprine (Imuran). Immune modifiers may work by causing a

reduction in the lymphocyte count (a type of white blood cell). Their onset of action is relatively slow (typically 2-3 months).

If you are taking immune modifiers, your blood cell count will be monitored on a regular basis because the immune modifiers can cause a significant reduction in the number of white blood cells, predisposing you to serious infections. Anti-TNF agent

Infliximab (Remicade) is an anti-TNF agent. TNF is produced by white blood cells and is believed to be responsible for promoting the tissue damage noted in persons with Crohn's disease. Infliximab acts by binding to TNF, thereby inhibiting its effects on the tissues. Infliximab is also used for the treatment of fistulae, a complication of Crohn's disease. Closure of fistulae has been reported in 68% of persons treated with infliximab. Infliximab must be given intravenously. It is very expensive, so insurance coverage may play a factor in the decision to use this drug. Antibiotics Metronidazole and ciprofloxacin are the most commonly used antibiotics in persons with IBD. Symptomatic treatments: You may be given antidiarrheal agents, antispasmodics, and acid suppressants for symptomatic relief. Experimental agents.

Drugs used in Crohn's disease include methotrexate, thalidomide, and interleukin-11. Drugs used in ulcerative colitis include cyclosporine A, nicotine patch, butyrate enema, and heparin. Surgical management Surgical treatment in persons with inflammatory bowel disease varies, depending upon the disease. Ulcerative colitis is a surgically curable disease because the disease is limited to the colon. However, surgical resection is not curative in persons with Crohn's disease. On the contrary, excessive surgical intervention in persons with Crohn's disease can lead to more problems. Situations arise in Crohn's disease in which

surgery without resection can be used. This is done to halt function of the colon in order possibly to allow for healing of the disease distal to the site where surgery is done. Ulcerative colitis

In about 25-30% of persons with ulcerative colitis, medical treatment is not completely successful. In such persons and in persons with dysplasia (changes in the cells that are considered a precursor to cancer), surgery may be considered. Unlike Crohn's disease, which can recur after surgery, ulcerative colitis is cured after colectomy(surgical removal of the colon). The surgical options for persons with ulcerative colitis depend on a number of factors: the extent of the disease, the person's age, and his overall health. The first option involves the removal of the entire colon and rectum (proctocolectomy) with the creation of an opening on the abdomen through which feces is emptied into a pouch (ileostomy). This pouch is attached to the skin with an adhesive. The other most commonly used option is a technically demanding surgery and is generally a multistage procedure. The surgeon removes the colon, creates an internal ileal pouch from the small intestine, attaches it to the anal sphincter muscle (ileoanal anastomosis), and creates a temporary ileostomy. After the ileoanal anastomosis heals, the ileostomy is closed and the passage of the feces through the anus is reestablished. Crohn's disease

Even though surgery is not curative in persons with Crohn's disease, approximately 75% of persons will require surgery at some point of time (especially for complications). The most simple surgery for Crohn's disease is the segmental resection, in which a segment of intestine with active disease or a stricture (narrowing) is removed and the remaining bowel is reanastomosed (two ends of healthy bowel are joined together). In persons with a very short stricture, instead of removal of that part of the intestine, a bowel-sparing stricturoplasty (repair) can be performed. Ileorectal or ileocolonic anastomosis is an option is some persons who have lower small intestine or upper colon disease. In persons with severe perianal fistulae, diverting ileostomy/colostomy is a surgical option. In this procedure, the function is halted for the distal colon and a temporary ileostomy or colostomy is created. The rectum, for which

function is halted, is allowed to heal, and the ileostomy/colostomy is then reversed.

Nursing management:Nursing intervention with rationale: 1. Observe and record stool frequency, characteristics, amount, and precipitating factors. Rationale: Helps differentiate individual disease and assesses severity of episode. 2. Promote bedrest and provide bedside commode.

Rationale: Rest decreases intestinal motility and reduces the metabolic rate when infection or hemorrhage is a complication. Urge to defecate may occur without warning and be uncontrollable, thus increasing risk of incontinence and falls if facilities are not close at hand.

3. Remove stool promptly. Provide room deodorizers. Rationale: Reduces noxious odors to avoid undue client embarrassment.

4. Identify foods and fluids that precipitate diarrhea, such as raw vegetables and fruits, whole-grain cereals, condiments, carbonated drinks, and milk products. Rationale: Avoiding intestinal irritants promotes intestinal rest.

5. Restart oral fluid intake gradually. Offer clear liquids hourly and avoid cold fluids. Rationale: Provides colon rest by omitting or decreasing the stimulus of foods and fluids. Gradual resumption of liquids may prevent cramping and recurrence of diarrhea; however, cold fluids can increase intestinal motility.

6. Provide opportunity to vent frustrations related to disease process. Rationale: Presence of disease with unknown cause that is difficult to cure and that may require surgical intervention can lead to stress reactions that may aggravate condition.

7. Observe for fever, tachycardia, lethargy, leukocytosis, decreased serum protein, anxiety, and prostration. Rationale: May signify that toxic megacolon or perforation and peritonitis are imminent or have occurred, necessitating immediate medical intervention.

8. Administer medications, as indicated: Antidiarrheals, such as diphenoxylate (Lomotil), loperamide (Imodium), and anodyne suppositories Rationale: Decreases GI motility or propulsion (peristalsis) and diminishes digestive secretions to relieve cramping and diarrhea. Note: Use with caution in UC because they may precipitate toxic megacolon.

9. Anti-inflammatories, such as mesalamine (Pentasa, Asacol); mesalaminecontaining drugs, for example, sulfasalazine (Azulfidine); and aminosalicylates, drugs that contain 5- aminosalicyclic acid (5-ASA), such as olsalazine (Dipentum) and balsalazide (Calazal) Rationale: Most people with mild or moderate ulcerative colitis are treated first with the group of drugs containing mesalamine, a substance that helps control inflammation. Sulfasalazine is the most commonly used of these drugs. Clients who do not benefit from it or who cannot tolerate it may receive 5-ASA agents, which are given orally, through an enema, or in a suppository, depending on the location of the inflammation in the colon. 10. Steroids, such as adrenocorticotropic hormone (ACTH), hydrocortisone (Cortenema, Cortifoam), prednisolone (Delta-Cortef), and prednisone (Deltasone) Rationale: Decreases acute inflammatory process. Steroid enemas (Cortenema) may be given in mild to moderate disease to aid absorption of the drug possibly with atropine sulfate or belladonna suppository. Current research suggests an 8-week course of time-release steroids may effect remission in Crohns disease; however, steroids are contraindicated if intra-abdominal abscesses are suspected.

Prevention No known dietary or lifestyle change prevents the development of inflammatory bowel disease. Dietary manipulation may help symptoms in persons with ulcerative colitis, and it actually may help reduce inflammation in Crohn's disease. However, there is no evidence that consuming or avoiding any particular food item causes or avoids flare-ups of IBD.

Smoking cessation is the only lifestyle change that may benefit persons with Crohn's disease. Smoking has been linked to increases in the number and severity of flare-ups of Crohn's disease. Smoking cessation occasionally is sufficient to make a person with refractory (not responding to treatment) Crohn's disease go into remission. Intestinal complications :

Profuse bleeding from the ulcers Perforation (rupture) of the bowel Strictures and obstruction: In persons with Crohn's disease, strictures often are inflammatory and frequently resolve with medical treatment. Fixed or fibrotic (scarring) strictures may require endoscopic or surgical intervention to relieve the obstruction. In ulcerative colitis, colonic strictures should be presumed to be malignant (cancerous). Fistulae (abnormal passage) and perianal disease: These are more common in persons with Crohn's disease. They may not respond to vigorous medical treatment. Surgical intervention often is required, and there is a high risk of recurrence. Toxic megacolon (acute non-obstructive dilation of the colon): This is a lifethreatening complication of ulcerative colitis and requires urgent surgical intervention. It is fortunately relatively rare. Malignancy: The risk of colon cancer in ulcerative colitis begins to rise significantly above that of the general population after approximately 8-10 years of diagnosis.

SMALL BOWEL
Definition

OBSTRUCTION

Small bowel obstruction means the small intestine is partially or totally blocked. When this happens, the contents of the intestine cannot properly get out of the body. Stools, fluid, and gas build up inside the intestine. This is a potentially serious condition that requires urgent medical care.

Causes Bowel obstruction may be caused by a mechanical problem. In this case, something inside the body blocks the movement of material through the intestine. Bowel obstruction can also be caused by an ileus, which is when the bowel itself does not work right. This nonmechanical type of obstruction is called paralytic ileus , or pseudo-obstruction. It is often the cause of obstruction in infants and children. Mechanical small bowel obstruction has many possible causes, including:

Hernias Scar tissue left behind by operations (adhesions) Gallstones (rarely) Crohns disease (an inflammatory bowel condition) Small bowel tumor Abnormal growth of tissue adjacent to the small bowel Folding in the wall of the intestine ( intussusception ) Twisted intestine (volvulus) Foreign bodies (items that were swallowed and got stuck)

Paralytic ileus may be caused by:

Medications, especially narcotics Infection in the lining of the small bowel (eg, intestinal flu in older children) Decreased blood supply to the small bowel Abdominal, joint, or spine surgery Kidney disease Long-standing diabetes

Risk Factors A risk factor is something that increases your chance of getting a disease or condition. The following factors increase chances of developing small bowel obstruction.

Hernia Crohns disease Cancer

Abdominal surgery Swallowing a foreign body

Symptoms If you experience any of these symptoms, do not assume it is due to a small bowel obstruction. These symptoms may be caused by other, less serious health conditions. However, if they are severe or persistent, consult your doctor. In the case of small bowel obstruction, symptoms often occur in combination. The symptoms for mechanical small bowel obstruction include:

Abdominal fullness and/or excessive gas Abdomen feels stretched out more than normal (abdominal distention) Pain and cramps in stomach area Vomiting Constipation (cannot pass gas or stool) Diarrhea Bad breath

The symptoms of paralytic ileus include:

Abdominal fullness and/or excessive gas Abdominal distention Vomiting after eating Pain is often less severe than in "mechanical small bowel obstruction

Diagnosis The exam will include listening for bowel sounds in your stomach. Very high pitched bowel sounds heard through a stethoscope suggest mechanical bowel obstruction, whereas paralytic ileus often produces no bowel sounds. Tests may include the following:

CT scan a type of x-ray that uses a computer to produce images of structures inside the abdomen Abdominal ultrasound the use of high-pitched sounds waves to produce images inside the abdomen

Abdominal x-ray the use of radiation to take a picture of structures inside the abdomen

Treatment

Fluid replacement with aggressive intravenous (IV) resuscitation using isotonic saline or lactated Ringer solution is indicated. Oxygen and appropriate monitoring are also required. Antibiotics are used to cover gram-negative and anaerobic organisms. In addition, analgesia and antiemetic are administered as indicated clinically. As previously mentioned, a nonoperative trial of as many as 3 days is warranted for partial or simple obstruction. Resolution of obstruction occurs in virtually all patients with these lesions within 72 hours.

Antibiotics These agents are for prophylaxis in surgical intervention, if needed. Cefazolin is a first-generation semisynthetic cephalosporin that arrests bacterial cell wall synthesis, inhibiting bacterial growth. Cefoxitin is a second-generation cephalosporin indicated for gram-positive cocci and gram-negative rod infections. Infections caused by cephalosporin- or penicillin-resistant gram-negative bacteria may respond to cefoxitin. Cefotetan is a second-generation cephalosporin indicated for infections caused by susceptible gram-positive cocci and gram-negative rods. Dosage and route of administration depend on the condition of patient, the severity of infection, and the susceptibility of the causative organism. Cefuroxime is a second-generation cephalosporin that maintains the grampositive activity of first-generation cephalosporins; it adds activity against Proteus mirabilis, Haemophilus influenzae, E coli, Klebsiella pneumoniae, and Moraxella catarrhalis. The condition of the patient, the severity of the infection, and the susceptibility of the microorganism determine the proper dose and route of administration. Meropenem is a bactericidal, broad-spectrum carbapenem antibiotic that inhibits cell-wall synthesis. It is effective against most gram-positive and gramnegative bacteria. Antiemetic These agents should be administered for symptomatic relief, usually in conjunction with GI decompression via placement of an NG tube for suction. Promethazine (Phenergan, Phenadoz, Promethegan) Promethazine is for the symptomatic treatment of nausea and vomiting. It is an antidopaminergic agent that is effective in treating emesis. Promethazine blocks postsynaptic mesolimbic dopaminergic receptors in the brain and reduces stimuli to the brainstem reticular system. Ondansetron is a selective 5-HT3-receptor antagonist that blocks serotonin peripherally and centrally; it is used in the prevention of nausea and vomiting. Ondansetron is metabolized in the liver through the P-450 pathway. Analgesics

Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary toilet, and have sedating properties, which are beneficial for patients who experience pain. Surgery Surgery is often required to relieve mechanical blockages, particularly those associated with cancer, scar tissue, and hernias. If small bowel obstruction is present, expect to be hospitalized. Treatment options include: Nursing management Nursing implication for intestinal obstruction. (1) Abdominal girths should be measured daily. For accuracy of comparison, follow these suggested guidelines: (a) Use the same measuring tape each time. (b) Place the patient in the same position each time. (c) Ensure that the tape measure is placed in the same position each time. This can be done by drawing small tic marks on the patient's abdomen to indicate position for the tape. (d) Measure the patient at the same time each day. (2) Note the color and character of all vomitus. Test for the presence of occult blood. (3) Any stool passed should be tested for the presence of occult blood. (4) Monitor vital signs closely. Elevations of temperature and pulse may indicate infection or necrosis. (5) Monitor I&O closely. Fluid and electrolyte losses must be replaced. Prevention There are no known ways to prevent small bowel disease, except, of course, avoiding nonedible foreign substances that could get stuck.

Possible Complications Complications may include or may lead to:

Electrolyte imbalances Infection Jaundice Perforation (hole) in the intestine

If the obstruction blocks the blood supply to the intestine, the tissue may die, causing infection and gangrene. Risk factors for tissue death include intestinal cancer, Crohn's disease, hernia, and previous abdominal surgery. In the newborn, paralytic ileus that is associated with destruction of the bowel wall (necrotizing enterocolitis) is life-threatening and may lead to blood and lung infections.

Conclusion So, here we conclude by saying that small intestinal disorders can be prevented by changes in the lifestyle and behaviour because these are the root causes of gastrointestinal disorders and small intestinal disorders. So, prompt treatment and prevention of further complications is the chief role of nurse. Hence as we have this knowledge we can apply this in our clinical practice. REFERENCES 1. B.D. Chaurasias (2004). Human Anatomy, 4th edition CBS publisher and distributer NEW DELHI; volume -1; Pp.265-272. 2. Brunner & Suddarth (2009), Text book of Medical Surgical Nursing : 11th edition Wolters kluwer, Lippincott Williams & Wilkins, Volume-1; Pp.723-739. 3. Joycee M. Black ,Jane Hokinson, Howks (2005), Medical surgical nursing: 7th edition Philadelphia : W.B. Saunders. 4. Lewis, Heilkemper, Dirksen, OBrien, Buchers (2007), Medical Surgical Nursing , 7th edition Mosby Elsevier ; Pp. 543-55
5.

Lippincott (2006), Mannual of Nursing Practice, 8th edition JP Indian

edition Lippincott Williams & wilkins ; Pp-216-219

Use of Probiotics in Gastrointestinal Disorders Probiotics are being used with increasing frequency as a treatment for several medical conditions, such as allergic diseases (atopic dermatitis, possibly allergic rhinitis), bacterial vaginosis, urinary tract infections, and prevention of dental caries or respiratory infections. Probiotics are used as a treatment for a variety of gastrointestinal (GI) disorders. In this review, the historical perspectives, proposed mechanisms of action, formulations and delivery systems, safety, and specific GI disorders for which probiotics have been used are discussed . They may restore normal bacterial microflora and effect the functioning of the GI tract by a variety of mechanisms. Probiotics are not currently regulated and only few randomized controlled trials exist investigating their efficacy in different GI disorders. They are available in a variety of formulations and delivery systems making interpretation and comparison of studies even more difficult. The efficacy of probiotics, either as a single strain or a combination of probiotics, has been tested in antibiotic-associated diarrhea, Clostridium difficile colitis, infectious diarrhea, ulcerative colitis, Crohn's disease, pouchitis, and irritable bowel syndrome, among other disorders.