Gastointestinal diseases

Gastointestinal diseases

1.      Crohn Disease

·         The exact cause of inflammatory bowel disease (IBD) is unknown, although there are components that appear to be infectious and other components that suggest immune dysregulation.

·         Ulcerative colitis and Crohn disease

·         Genetic variations explain some of the increased risk of disease occurrence.

·         The severity of Crohn’s disease can be assessed by the Crohn’s disease activity index, which includes stool frequency, presence of blood in stool, endoscopic appearance, and physician’s global assessment.

·         The goals of treatment of IBD are resolution of acute inflammation and complications, alleviation of systemic manifestations, maintenance of remission, and in some patients, surgical palliation or cure.

2.      GERD

·         Symptoms, such as heartburn,and for signs and symptoms of complications that require immediate medical attention, such as dysphagia or bleeding.

·         Endoscopy is used to evaluate mucosal damage from gastroesophageal reflux disease (GERD) and assess for the presence of Barrett’s esophagus (BE); 24-hour ambulatory pH testing or a therapeutic trial of a proton pump inhibitor are useful for diagnosing GERD in patients with persistent symptoms or atypical symptoms; manometry is useful in evaluating motility and before antireflux surgery.

·         The goals of treatment of GERD are to alleviate symptoms,to decrease the frequency of recurrent disease, to promote healing of mucosal injury, and to prevent complications.

·         Patient medication profiles should also be reviewed for drugs that may aggravate GERD. Patients should be monitored for adverse drug reactions and potential drug-drug interactions of drugs used to treat GERD. Finally, patients should be assessed for compliance to their therapeutic regimen.

3.      IBS (Irritable Bowel Syndrome)

·         Irritable bowel syndrome is one of the most common gastrointestinal disorders, and is characterized by lower abdominal pain, disturbed defecation, and bloating. Many nongastrointestinal manifestations also exist with IBS. Recent studies have found that visceral hypersensitivity is a major culprit in the pathophysiology of the disease.

·         IBS results from altered somatovisceral and motor dysfunction of the intestine from a variety of causes. Abnormal central nervous system processing of afferent signals may lead to visceral hypersensitivity, with the specific nerve pathway affected determining the exact symptomatology expressed. This visceral hypersensitivity is a neuroenteric phenomenon that is independent of motility and psychological disturbances.

·         Factors known to contribute to these alterations include genetics, motility factors, inflammation, colonic infections, mechanical irritation to local nerves, and psychological factors

4.      Ileus Paralysis

·         Paralysis of the intestine. The intestinal paralysis need not be complete, but it must be sufficient to prohibit the passage of food through the intestine and lead to intestinal blockage.

·         Paralytic ileus is a common aftermath of some types of surgery. It can also result from certain drugs and from various injuries and illnesses. Paralytic ileus causes constipation and bloating. On listening to the abdomen with a stethoscope, no bowel sounds are heard because the bowel is inactive

5.      Cirrhosis

o   Cirrhosis is a severe, chronic, irreversible disease associated with significant morbidity and mortality. However, the progression of cirrhosis secondary to alcohol abuse can be interrupted by abstinence. It is therefore imperative for the clinician to educate and support abstinence from alcohol as part of the overall treatment strategy of the underlying liver disease.

o   Cirrhosis is defined as a diffuse process characterized by fibrosis and a conversion of the normal hepatic architecture into structurally abnormal nodules.

o   Regardless of the mechanism of injury, the end result is the destruction of hepatocytes and their replacement with fibrous tissue. As fibrotic tissue replaces normal hepatic parenchyma, resistance to blood flow results in the clinical problems of portal hypertension and the development of varices and ascites

o   Hepatocyte loss and intrahepatic shunting of blood results in diminished metabolic and synthetic function, which leads to hepatic encephalopathy and coagulopathy

6.      Cholelithiasis

·         the presence of stones in the gallbladder or bile ducts

·         gallstones may be caused by a combination of factors, including inherited body chemistry, bw, gallbladder motility (movement), and perhaps diet.

·         Cholesterol gallstones develop when bile contains too much cholesterol and not enough bile salts. Besides a high concentration of cholesterol, two other factors seem to be important in causing gallstones. The first is how often and how well the gallbladder contracts; incomplete and infrequent emptying of the gallbladder may cause the bile to become overconcentrated and contribute to gallstone formation. The second factor is the presence of proteins in the liver and bile that either promote or inhibit cholesterol crystallization into gallstones.

·         In addition, increased levels of the hormone estrogen as a result of pregnancy, hormone therapy, or the use of combined (estrogen-containing) forms of contraception, may increase cholesterol levels in bile and also decrease gallbladder movement, resulting in gallstone formation.