Disorder of GI tract Dr Zainab Sajid AlShimmari

Disorder of GI tract Dr. Zainab Sajid Al-Shimmari

Disorders of GI tract: Peptic ulcers: The term peptic ulcer refers to erosion of the mucosa lining any portion of the G. I. tract. If the ulcer occurs in the stomach lining, it is specifically referred to as a gastric ulcer. In the United States most ulcers occur in the duodenum and in elderly patients.

The causes : of peptic ulcer disease include the following: 1 • Infection with the bacteria Helicobacter pylori. H. pylori infection impairs the protective mechanisms of the G. I. tract against low p. H and digestive enzymes and leads to ulceration of the mucosa. 2 • Stress — Emotional, trauma, surgical. 3 • Injury or death of mucus-producing cells. 4 • Excess acid production in the stomach. 5 • Chronic use of aspirins.

Here is a much larger 3 x 4 cm gastric ulcer that led to the resection of the stomach shown here. This ulcer is much deeper with more irregular margins. Complications of gastric ulcers (either benign or malignant)include pain, bleeding, perforation, and obstruction

Microscopically, the ulcer here is sharply demarcated, with normal gastric mucosa on the left falling away into a deep ulcer whose base contains inflamed, necrotic debris. An arterial branch at the ulcer base is eroded and bleeding

Gastritis is often accompanied by infection with Helicobacter pylori. This small curved to spiral rod-shaped bacterium is found in the surface epithelial mucus of most patients with active gastritis. The rods are seen here with a methylene blue stain.

Zollinger–Ellison syndrome: 1 • Tumors of the gastrin-secreting endocrine cells of the pancreas or, less frequently, the duodenal wall. 2 • Leads to excessive acid production by the G. I. tract. 3 • Development of serious and aggressive peptic ulcers. 4 • Formation of ulcers in atypical locations. 5 • Complications can include perforation, hemorrhage and obstruction.

Manifestations of peptic ulcer disease: 1 • Pain that for duodenal ulcers is often relieved by eating or antacids. 2 • G. I. bleeding and possible hemorrhage (20 to 25% of patients). 3 • Perforation of ulcers with significant mortality. 4 • Obstruction of G. I. tract.

Irritable bowel syndrome: 1 • May be one of the most common G. I. disorders. 2 • Patients present with symptoms of G. I. pain, gas, bloating and altered bowel function (diarrhea or constipation). Most symptoms are localized to the lower intestine and colon. 3 • No underlying pathophysiologic processes have yet to be identified in these patients. “Hyperreactivity” and excessive motility of the bowels may be contributing factors. 4 • Emotional factors and diet may exacerbate the symptoms.

Crohn’s disease: 1 • Although the exact etiology of Crohn’s disease in unknown, there appears to be a significant autoimmune component. 2 • The disease may affect any region of the G. I. tract but is most commonly seen in the distal ileum and colon. 3 • The inflammation of Crohn’s disease is particularly evident in the Submucosal layer of the intestine. The pattern of inflammation seen is a granulomatous inflammation with distinct “cobblestone” appearance to the mucosa. The inflammatory lesions are not constant along the length of the intestine but rather present with a “skip” pattern that intersperses areas of inflammation with normal looking, noninflamed tissue.

This is example of Crohn's disease involving the small intestine. Here, the mucosal surface demonstrates an irregular nodular appearance with hyperemia and focal superficial ulceration.

Microscopically, Crohn's disease is characterized by transmural inflammation. Here, inflammatory cells (the bluish infiltrates) extend from mucosa through submucosa and muscularis and appear as nodular infiltrates on the serosal surface with pale granulomatous centers.

-At high magnification the granulomatous nature of the inflammation of Crohn's disease is demonstrated here with epithelioid cells, giant cells, and many lymphocytes. Special stains for organisms are negative

Manifestations of Crohn’s disease: 1 • Diarrhea (blood is usually not evident in the stool but may be occult, i. e. , detected by clinical assay). 2 • Intestinal pain similar to indigestion. 3 • Fever. 4 • Weight loss from intestinal malabsorption. 5 • Nausea, anorexia, vomiting. 6 • Complications: intestinal obstruction, formation of fistulas (abnormal connections between the colon and other abdominal organs). 7. Toxic megacolon.

Diarrhea: 1 -The usual definition of diarrhea is excessively frequent passage of stools. Diarrhea can be acute or chronic. Diarrhea is considered to be chronic when the symptoms persist for 3 weeks in children or adults and 4 weeks in infants. 2 - In developing countries, diarrhea is a common cause of mortality among children less than 5 years of age, with an estimated 2 million deaths annually. The complaint of diarrhea is a general one and can be related to a number of pathologic and non pathologic factors.

3 -Diarrhea can be acute or chronic and can be caused by infectious organisms, food intolerance, drugs, or intestinal disease. (i)Acute diarrheas that last less than 4 days are predominantly caused by infectious agents and follow a self-limited course. (ii)- Chronic diarrheas are those that persist for longer than 3 to 4 weeks. They often are caused by conditions such as inflammatory bowel disease, irritable bowel syndrome, malabsorption syndrome, endocrine disorders (hyperthyroidism, diabetic autonomic neuropathy), or radiation colitis.

4 -Diarrhea commonly is divided into two types, large volume and small volume, based on the characteristics of the diarrheal stool. Largevolume diarrhea results from an increase in the water content of the stool, and small-volume diarrhea results from an increase in the propulsive activity of the bowel. diarrhea is a combination of these two types.

I-Large-Volume Diarrhea. 1 -Large-volume diarrhea can be classified as secretory or osmotic, according to the cause of the increased water content in the feces. Water is pulled into the colon along an osmotic gradient (i. e. , osmotic diarrhea) or is secreted into the bowel by the mucosal cells (i. e. , secretory diarrhea). 2 -The large-volume form of diarrhea usually is a painless, watery type without blood or pus in the stools.

3 -In osmotic diarrhea, water is pulled into the bowel by the hyperosmotic nature of its contents. (i)- It occurs when osmotically active particles are not absorbed. In persons with lactase deficiency, the lactose in milk cannot be broken down and absorbed. (ii)-Magnesium salts, which are contained in milk of magnesia and many antacids, are poorly absorbed and cause diarrhea when taken in sufficient quantities. (iii)-Another cause of osmotic diarrhea is decreased transit time, which interferes with absorption. Osmotic diarrhea usually disappears with fasting.

4 -Secretory diarrhea occurs when the secretory processes of the bowel are increased. A- Most acute infectious diarrheas are of this type. Enteric organisms cause diarrhea by several ways. Some are noninvasive but secrete toxins that stimulate fluid secretion (e. g. , Vibrio cholerae, pathogenic E. coli, and rotavirus). B - Others (e. g. , Shigella, Salmonella, Yersinia, and Campylobacter) invade and destroy intestinal epithelial cells, thereby altering fluid transport so that secretory activity continues while absorption activity is halted.

C- Diarrhea with vomiting and fever suggests food poisoning, often caused by staphylococcal enterotoxin. D-Secretory diarrhea also occurs when excess bile acids remain in the intestinal contents as they enter the colon. This often happens with disease processes of the ileum because bile salts are absorbed there. E- It also may occur with bacterial overgrowth in the small bowel, which interferes with bile absorption. Some tumors, such as those of the Zollinger-Ellison syndrome and carcinoid syndrome, produce hormones that cause increased secretory activity of the bowel.

II-Small-Volume Diarrhea. 1 -Small-volume diarrhea commonly is associated with acute or chronic inflammation or intrinsic disease of the colon, such as ulcerative colitis or Crohn disease. 2 -Small-volume diarrhea usually is evidenced by frequency and colicky abdominal pain. It commonly is accompanied by tenesmus (i. e. , painful straining at stool), fecal soiling of clothing, and awakening during the night with the urge to defecate.

Gallstone formation (cholelithiasis): 1 • The gallstones that form in the gall bladder are hardened precipitates of bile that contain predominantly cholesterol. 2 • The size of gallstones can range from the size of a grain of sand to several inches in diameter. 3 • Factors such as aging, excess cholesterol, obesity, sudden dietary changes or abnormal fat metabolism may contribute to gallstone formation. 4 • Gallstones may be detected by a number of techniques including radiography, ultrasonography and cholecystoscopy.

Gall bladder: Stone formation.

Manifestations of gallstone formation. 1 • Symptoms of gallstone formation will generally not occur until the stones have reached sufficient size to block the bile ducts. 2 • Acute and severe abdominal pain. 3 • Nausea, vomiting, fever, chills. 4 • Jaundice from obstruction of bile outflow.

Viral hepatitis: The term hepatitis refers to inflammation and possible injury of the liver. Hepatitis may be caused by a number of injurious agents such as viruses, alcohol, toxins and drugs. When the liver is inflamed and injured as a result of viral infection it is termed a viral hepatitis In the United States, there are three main hepatitis viruses, designated hepatitis A, B and C. Two other variants, hepatitis D and E are also present in certain populations. All of the hepatitis viruses target the hepatocytes of the liver as their site of infection and replication.

Functions of the Liver. 1 -Carbohydrate, fat and protein metabolism. 2 -Metabolism of steroid and sex hormones. 3 -Production of bile. 4 -Elimination of bilirubin. 5 -Drug metabolism. 6 -Synthesis of plasma proteins and clotting factors. 7 -Storage of glycogen, minerals and vitamins.

Epidemiology. 1. Hepatitis A. A • Transmitted via the fecal/oral route, usually through fecal-contaminated food, water or shellfish. The highest incidence occurs in children. B • The virus may also be transmitted via blood and contaminated blood products but this is not the primary means of transmission. 2. Hepatitis B. A • Blood-borne pathogen. B • Major routes of transmission include intravenous drug use, unprotected sexual contact and exposure to contaminated blood products.

9 -Grossly, there areas of necrosis and collapse of liver lobules seen here as ill-defined areas that are pale yellow. Such necrosis occurs with viral hepatitis.

The necrosis and lobular collapse is seen here as areas of hemorrhage and irregular furrows and granularity on the cut

3. Hepatitis C. A • Blood-borne pathogen. B • Major route of transmission is through contaminated blood and body fluids. C • Accounts for most cases of transfusion-related viral hepatitis. 4. Hepatitis D. A • Blood-borne pathogen. B • Can only infect individuals with active hepatitis B infection. C • Transmitted through contaminated blood and body fluids.

Manifestations of viral hepatitis: 1 • Range from asymptomatic to severe. 2 • Fatigue, malaise, anorexia, nausea. 3 • Jaundice. 4 • Liver inflammation and abdominal pain. 5 • Abnormal liver function and enzyme levels. 6 • Chronic active or persistent hepatitis can lead to progressive liver injury, liver failure and death. The chronic form of hepatitis is most common with hepatitis B, C, D, but rare with hepatitis A and E. 7 • Chronic active hepatitis is also associated with an increased incidence of hepatocellular carcinoma.

Hepatic Failure: I-Acute hepatic failure occurs most frequently in acute viral hepatitis. Other causes are hepatotoxic drug reactions (e. g. anaesthetic agents, nonsteroidal antiinflammatory drugs, anti-depressants), carbon tetrachloride poisoning, acute alcoholic hepatitis, mushroom poisoning and pregnancy complicated with eclampsia. II-Chronic hepatic failure is most often due to cirrhosis. Other causes include chronic active hepatitis, chronic cholestasis (cholestatic jaundice) and Wilson’s disease.

MANIFESTATIONS 1. Jaundice. A-Jaundice usually reflects the severity of liver cell damage since it occurs due to failure of liver cells to metabolise bilirubin. BIn acute failure such as in viral hepatitis, jaundice nearly parallels the extent of liver cell damage, while in chronic failure such as in cirrhosis jaundice appears late and is usually of mild degree.

2. Hepatic encephalopathy (Hepatic coma. A- The genesis of CNS manifestations in liver disease is by toxic products not metabolised by the diseased liver. The toxic products may be ammonia and other nitrogenous substances from intestinal bacteria which reach the systemic circulation without detoxification in the damaged liver and thus damage the brain. B-Advanced cases of hepatic coma have poor prognosis but may respond favourably to hepatic transplantation.

3. Hyperkinetic circulation. A-All forms of hepatic failure associated with a hyperkinetic circulation characterised by peripheral vasodilatation, increased blood flow and increased cardiac output. B-There is increased splenic flow but reduced renal blood flow resulting in impaired renal cortical perfusion. These changes result in tachycardia, low blood pressure and reduced renal function.

4. Hepato renal syndrome. A -The term hepatorenal syndrome is applied to patients of both acute and chronic hepatic failure who develop renal failure. BHepatorenal syndrome develops in about 10% cases of acute and chronic liver diseases. The acute renal failure is usually associated with oliguria and uraemia but with good tubular function. The histology of kidney is virtually normal, suggesting functional defect for the renal failure.

5. Hepatopulmonary syndrome. The pulmonary changes in chronic hepatic failure such as in cirrhosis consist of pulmonary vasodilatation with intra-pulmonary arteriovenous shunting. This results in ventilation-perfusion inequality that may lead to impaired pulmonary function, and cyanosis. 6. Coagulation defects. Impaired synthesis of a number of coagulation factors by the diseased liver may result in coagulation disorders. These include disseminated intravascular coagulation, thrombocytopenia and presence of fibrin degradation products in the blood.

7. Ascites and oedema. Chronic liver failure due to cirrhosis may result in portal hypertension and ascites. Decreased synthesis of albumin by the liver resulting in hypoproteinaemia and consequent fall in plasma oncotic pressure, increased hydrostatic pressure due to portal hypertension and secondary hyperaldosteronism, contribute to the development of ascites and oedema in these patients.

8. Endocrine changes may be found in association with chronic hepatic failure. The changes are more common in alcoholic cirrhosis in active reproductive life. In the male, the changes are towards feminisation such as gynaecomastia and hypogonadism. In the female, the changes are less towards masculinisation but atrophy of gonads and breasts occurs.

9. Skin changes. In alcoholic cirrhosis ‘arterial spiders’having radiating small vessels from a central arteriole are frequent in the vascular region drained by superior vena cava such as in the neck, face, forearms and dorsum of hands. 10. Foetor hepaticus. A sweetish smell of the breath is found in severe cases of acute and chronic hepatocellular diseases. It appears to be of intestinal origin, possibly due to failure of the liver to detoxify sulfur-containing substances absorbed from the gut.

Primary biliary cirrhosis. 1. The condition is predominant in middle-aged women (male: female ratio = 1: 9) and has led to the suggestion of a possible endocrine origin. 2. Familial incidence has been observed suggesting the role of some genetic influence. 3. There is elevated cholesterol level with appearance of xanthoma and xanthelasma. Hepatomegaly and chronic liver disease are late features of the disease.

4. the most widely accepted hypothesis is autoimmune origin of the disease. In support are the following observations: increased incidence of associated autoimmune diseases (e. g. autoimmune thyroiditis), a-circulating anti-mitochondrial antibody of Ig. G class detected in more than 90% cases; b-elevated levels of immunoglobulins, particularly of Ig. M. c-increased levels of circulating immune complexes. d-decreased number of circulating T-cells. e-accumulation of T cells around bile ducts.

MANIFESTATIONS. 1 -Primary biliary cirrhosis may remain asymptomatic for months to years. The patients present with dark urine, pale stools, steatorrhoea, jaundice and skin pigmentation. 2 -The earliest laboratory finding is a markedly elevated serum alkaline phosphatase level. 3 -Elevation of serum lipids is accompanied by appearance of periorbital xanthelasma and xanthomas over joints. 4 - Death usually results from hepatic failure, variceal bleeding.

Celiac Disease: Celiac disease, also known as celiac sprue and glutensensitive enteropathy, is an immune-mediated disorder triggered by ingestion of gluten-containing grains (including wheat, barley, rye). 1 -The disease results from an inappropriate T-cell– mediated immune response against ingested α-gliadin (a component of gluten protein) in genetically predisposed people. More than 95% of people with celiac disease exhibit the gluten-derived gliadin peptides on its antigen-presenting grove to stimulate intestinal mucosal T cells.

2 - Persons with the disease have increased levels of antibodies to a variety of antigens, including transglutaminase, endomysium, and gliadin. The result immunologic response produces an intense inflammatory reaction that results in loss of absorptive villi from the small intestine. When the resulting lesions are extensive, they may impair absorption of macronutrients (i. e. , proteins, carbohydrates, fats) and micronutrients (i. e. , vitamins and minerals). Small bowel involvement is most prominent in the proximal part of the small intestine where the exposure to gluten is greatest.

Normal small intestinal mucosa is seen at the left, and mucosa involved by celiac sprue at the right. There is blunting and flattening of villi with celiac disease, and in severe cases a loss of villi with flattening of the mucosa as seen here.

3 -The classic form of celiac disease presents in infancy and manifests as failure to thrive, diarrhea, abdominal distention, and occasionally, severe malnutrition. Older children may present with constitutional short stature and dental enamel defects. 4 - In adults, gastrointestinal symptoms may manifest as diarrhea, constipation, or other symptoms of malabsorption such as bloating, flatus, or belching. A small percentage of adults with gluten-sensitive enteropathy may present with dermatitis herpetiformis. This skin condition, which is characterized by lesions that are very similar to those of herpes simplex.

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