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Patho Ch.34 study set

Terms in this set (19)

Diarrhea: Diarrhea is an increase in the frequency of defecation and in the fluid content and volume of feces. More than three stools per day are considered abnormal. Many factors determine stool volume and consistency, including water content of the colon and the presence of nonabsorbed food, nonabsorbable material, and intestinal secretions. Stool volume in the normal adult averages less than 200 g/day. Stool volume in children depends on age and size. An infant may pass up to 100 g/day. The adult intestine processes approximately 9L of luminal contents per day: 2 L is ingested and the remaining 7L consists of intestinal secretions. Of this volume, 99% of the fluid is absorbed: 90% (7-8 L) in the small intestine and 9% (1-2 L) in the colon. Normally, approximately 150 ml of water is excreted daily in the stool.
Patho: Diarrhea in which the volume of feces is increased is called large-volume diarrhea. It generally is caused by excessive amounts of water or secretions or both in the intestines. Small-volume diarrhea, in which the volume of feces is not increased, usually results from excessive intestinal motility. The three major mechanisms of diarrhea are osmotic, secretory, and motile:
1. Osmotic diarrhea. A nonabsorbable substance in the intestine draws excess water into the intestine and increases stool weight and volume, producing large-volume diarrhea. Causes include lactase and pancreatic enzyme deficiency; excessive ingestion of synthetic, nonabsorbable; full-strength tube-feeding formulas; or dumping syndrome associated with gastric resection.
2. Secretory diarrhea. Excessive mucosal secretion of fluid and electrolytes produces large-volume diarrhea. Infectious causes include viruses (e.g., rotavirus), bacterial enterotoxins (e.g., Eschericha coli and Vibrio cholerae), or exotoxins from overgrowth of Clostridum difficile following antibiotic therapy. Small-volume diarrhea is usually cause by an inflammatory disorder of the intestine, such as ulcerative colitis or Crohn disease, but can also result from fecal impaction.
3. Motility diarrhea. Food is not mixed properly, digestion and absorption are impaired, and motility is increased. Causes include resection of the small intestine (short bowel syndrome), surgical bypass of an area of the intestine or fistula formation between loops of intestine, irritable bowel syndrome-diarrhea predominant, excessive motility of the intestine caused by diabetic neuropathy and hyperthyroidism, and laxative abuse.

Constipation: Constipation is difficult or infrequent defecation. It is a common problem and usually means a decrease in the number of bowel movements per week, hard stools, and difficult evacuation, but the definition must be individually determined. Normal bowel habits range from one to three evacuations per day to one per week. Constipation can occur as a primary or secondary condition.
Patho: Primary constipation is generally classified into three categories: normal transit (functional) constipation involves a normal rate of stool passage but there is difficulty with stool evacuation; slow-transit constipation involves impaired colonic motor activity with infrequent bowel movements, straining to defecate, mild abdominal distension, and palpable stool in the sigmoid colon; and pelvic floor dysfunction (pelvic floor dysynergia) refers to an inability or difficulty expelling stool because of dysfunction of the pelvic floor muscles or anal sphincter.
Secondary constipation can be caused by neurologic disorders (e.g. stroke, Parkinson disease, spinal cord lesions, multiple sclerosis, Hirschspurg disease) in which neural pathways or neurotransmitters are altered and colon transit time delayed. A low-residual diet (the habitual consumption of highly refined foods) decreases the volume and number of stools and causes constipation. Activity stimulates peristalsis (involuntary constriction and relaxation of the muscles of the intestine) and a sedentary lifestyle and lack of regular exercise are common causes of constipation. Lack of access to toilet facilities, consistent suppression of the urge to empty the bowel, and dehydration are other causes. Opiates (particularly codeine), antacids containing calcium carbonate or aluminum hydroxide, anticholinergics, iron, and bismuth tend to inhibit bowel motility. Endocrine or metabolic disorders associated with constipation include hypothyroidism, diabetes mellitus, hypokalemia, and hypercalcemia. Pelvic hiatal hernia (herniation of the bowel through the floor of the pelvis), diverticuli, irritable bowel syndrome-constipation predominant, and pregnancy are associated with constipation. Aging may result in decreased mobility, changes in neuromuscular function, use of medications, and comorbid medical conditions causing constipation. Constipation as a notable change in bowel habits can be an indication of colorectal cancer.

Abdominal pain: Abdominal pain is the presenting symptom of a number of gastrointestinal diseases and can be acute or chronic. The casual manifestations of abdominal pain are mechanical, inflammatory, or ischemic. Generally, the abdominal organs are not sensitive to mechanical stimuli, such as cutting, tearing, or cruching. These organs are, however, sesitive to stretching and distention, which activates nerve endings in both hollow and solid structures. Pain accompanies rapid distension rather than gradual distention. Traction on the peritoneum caused by adhesions, distension of the common bile duct, or forceful peristalsis resulting from intestinal obstruction causes pain because of increased tension. Capsules that surround solid organs, such as the liver and gallbladder, contain pain fibers that are stimulated by stretching if these organs swell. Abdominal pain may be generalized to the abdomen or localized to a particular abdominal quadrant. The nature of the pain is often described as sharp, dull, or colicky. Abdominal pain is usually associated with tissue injury. Biochemical mediators of the inflammatory response, such as histamine, bradykinin, and serotonin, stimulate organic nerve endings and produce abdominal pain. The edema and vascular congestion that accompany chemical, bacterial, or viral inflammation also causes painful stretching. Hindrance of blood flow from the distention of bowel obstruction or mesenteric vessel thrombosis produces the pain of ischemia, and increased concentrations of tissue metabolites stimulate pain receptors. Abdominal pain can be parietal (somatic), visceral, or referred:
-Parietal pain, from the parietal peritoneum, is more localized and intense than visceral pain, which arises from the organs themselves. Parietal pain lateralizes because, at any particular point, the parietal peritoneum is innervated from only one side of the nervous system.
-visceral pain arises from a stimulous (distension, inflammation, ischemia) acting on an abdominal organ. It is usually poorly localized with a radiating pattern and may be referred pain. Visceral pain is diffuse and vague because nerve endings in abdominal organs are sparse and multisegmented. Pain arising from the stomach, for example, is experienced as a sensation of fulness, cramping, or gnawing in the midepigastric area.
-Referred pain is visceral pain felt at some distance from a diseased or affected organ. It is usually well localized and is felt in skin or deeper tissues that share a central afferent pathway with the affected organ. For example, acute cholecystitis may have pain referred to the right shoulder or scapula. Generally, referred pain develops as the intensity of a visceral pain stimulus increases.
Gastrointestinal bleeding: Upper gastrointestinal bleeding is bleeding in the esophagus, stomach, or duodenum, and is characterized by frank bright red bleeding or dark, grainy digested blood ("coffee ground") that has been affected by stomach acids (see table 34-1). Upper gastrointestinal bleeding is commonly caused by bleeding varices (varicose veins) in the esophagus, peptic ulcers, or a Mallory-Weiss tear at the esophageal/gastric junction caused by severe retching. Lower gastrointestinal bleeding, or bleeding from the jejunum, ileum, colon, or rectum, can be caused by polyps, diverticulitis, inflammatory disease, cancer, or hemorrhoids. Occult bleeding is usually caused by slow, chronic blood loss that is not obvious and results in iron deficiency anemia (low RBC's or hemoglobin) as iron stores in the bone marrow are slowly depleted. Acute, severe gastrointestinal bleeding is life-threatening, depending on volume and rate of blood loss, associated disease and age of the affected individual, and effectiveness of treatment. Physiologic response to gastrointestinal bleeding depends on the amount and rate of the loss (fig 34-1). Changes in blood pressure and heart rate are the best indicators of massive blood loss in the gastrointestinal tract. During early stages of blood volume depletion, the peripheral vascular compartment constricts to shunt blood to vital organs, including the brain. This is manifested as postural hypotension (a drop in blood pressure that occurs with a change from the recumbent position to a sitting or upright position), light-headedness, and loss of vision. Tachycardia develops as a compensatory response to maintain cardiac output and tissue perfusion. If blood loss continues, hypovolemic shock progresses (see ch. 23). Diminished blood flow to the kidneys causes decreased urine output and may lead to oliguria (low urine output), tubular necrosis, and renal failure. Ultimately, insufficient cerebral and coronary blood flow causes irreversible anoxia and death. The accumulation of blood in the gastrointestinal tract is irritating and increases peristalsis, causing vomiting or diarrhea, or both. If bleeding is from the lower gastrointestinal tract, the diarrhea is frankly bloody. Bleeding from the upper gastrointestinal tract also can be rapid enough to produce hematochezia (bright red stools), but generally some digestion of the blood components will have occured, producing melena-black or tarry stools that are sticky and have a characteristic foul odor. The digestion of blood proteins originating from massive upper gastrointestinal bleeding is reflected by an increase in blood urea nitrogen (BUN) levels (see fig 34-1). The hematocrit and hemoglobin values are not the best indicators of acute gastrointestinal bleeding because plasma volume and red cell volume are lost proportionately. As the plasma volume is replaced, the hematocrit and hemoglobin values begin to reflect the extent of blood loss. The interpretation of these values is modified to account for exogenous replacement of fluids and the hydration status of the tissues.
-Dysphagia: is difficulty swallowing. It can result from mechanical obstruction of the esophagus or a functional disorder that impairs esophageal motility.

-Achalasis: is a rare form of dysphagia characterized by loss of esophageal peristalsis (involuntary contraction of intestinal muscles) and failure of the lower esophageal sphincter (LES) to relax (functional obstruction.

-Gastroesophageal reflux disease (GERD): is the reflux of chyme (acid and pepsin) from the stomach through the lower esophageal sphincter to the esophagus.

-Nonerosive reflux disease (NERD): individuals have symptoms of reflux disease but no visible esophageal mucosal injury.

-Reflux esophagitis: individuals with combination of factors causing an inflammatory response to the reflux.

-Hiatal hernia: is a type of diaphragmatic hernia with protrusion (herniation) of the upper part of the stomach through the diaphragm and into the thorax (fig 34-3) The two most common types of hiatal hernia are as follows:
1. Sliding hiatal hernia: (most common) The stomach slides or moves into the thoracic cavity through the esophageal hiatus.
2. Paraesophageal hiatal hernia: The greater curvature of the stomach herniates through a secondary opening in the diaphragm and lies alongside the esophagus.

-Gastroparesis: delayed gastric emptying in the absence of mechanical gastric outlet obstruction, common in individuals with diabetes and dyspepsia (indigestion(pain or discomfort in the stomach associated with difficulty in digesting food))

-Pyloric obstruction: (gastric outlet obstruction) is the narrowing or blocking of the opening between the stomach and the duodenum.

-Intestinal obstruction: Can be caused by any condition that prevents the normal flow of chyme through the intestinal lumen.

-Paralytic ileus: (aka functional obstruction) is a failure of intestinal motility often occurring after surgery
Pyloric obstruction clinical manifestations:
Early in the course of pyloric obstruction, the individual experiences vague epigastric fullness, which becomes more distressing after eating later in the day. Nausea and epigastric (upper central region of the abdomen) pain may occur as the muscles of the stomach contract in attempts to force chyme past the obstruction. These symptoms disappear when the chyme finally moves into the duodenum. As obstruction progresses, anorexia develops, sometimes accompanied by weight loss. Severe obstruction causes gastric distension and atony (lack of muscle tone and gastric motility). Gastric distention stimulates gastric secretion, which increases the feeling of fullness. Rolling or jarring of the abdomen produces a sloshing sound called the succussion splash. At this stage, vomiting is a cardinal sign of obstruction. It is usually copious and occurs several hours after eating. The vomitus contains undigested food but no bile. Prolonged vomiting leads to dehydration, which is accompanied by a hypokalemic and hypochloremic metabolic aclkalosis caused by loss of potassium and gastric acid. Because food does not enter the intestine, stools are infrequent and small. Prolonged pyloric obstruction causes malnutrition, dehydration, and extreme debilitation.

Intestinal Obstruction and paralytic ileus clinical manifestations:
Crampy/colicky pains followed by vomiting and distention are the cardinal symptoms of small bowel obstruction. Colonic obstruction usually presents as hypogastric pain and abdominal distension. Typically the pain occurs intermittently and intensifies for seconds or minutes as a peristalic wave of muscle contraction meets the obstruction. Sweating, nausea, and hypotension occur as an autonomic response. The passing of the wave is followed by a pain-free interval. With severe distention, the pain may diminish in intensity. If strangulation occurs, the pain loses its colicky character, becoming more constant and severe as ischemia progresses to necrosis, perforation, and peritonitis. Vomiting and distension vary, depending on the level of the obstruction. Obstruction at the pylorus causes early, profuse vomiting of clear golden-yellow gastric fluid. Obstruction in the proximal small intestine causes mild distention and vomiting of bile-stained (green to brown) fluid. Obstruction lower in the intestine causes more pronounced distention, and vomiting may not occur or may occur later and contain fecal material. Partial obstruction can cause diarrhea or constipation, but complete obstruction usually causes constipation only. Early in the course of complete obstruction, the frequency of bowel sounds increases and they may be tinkly and accompanied by peristaltic rushes and crampy/colicky abdominal pain as the bowel contracts to overcome the obstruction. During advanced stages of bowel obstruction the abdomen will become distended and silent. Distention may be severe enough to push against the diaphragm and decrease lung volume. This can lead to atelectasis and pneumonia, particularly in debilitated individuals. Signs of dehydration, hypovolemia, and metabolic acidosis may be observed as early as 24 hours after the occurance of complete obstruction.
Gastritis is an inflammatory disorder of the gastric mucosa. It can be acute or chronic and affect the fundus or antrum, or both. Acute gastritis erodes the surface epithelium in a diffuse or localized pattern. The erosions are typically superficial. Acute gastritis is usually the result of injury of the protective mucosal barrier caused by drugs or chemicals. Nonsteroidal anti inflammatory drugs (NSAIDs) that inhibit the action of cyclooxygenase-1 (COX-1) cause gastritis, perhaps because they inhibit prostaglandins, which normally stimulate the secretion of mucus. Alcohol, histamine, digitalis, and metaabolic disorders such as uremia (A condition involving abnormally high levels of waste products in the blood) are contributing factors. The clinical manifestations of acute gastritis can include vague abdominal discomfort, epigastric tenderness, and bleeding. Healing usually occurs spontaneously within a few days. Discontinuing injurious drugs, using antacids, or decreasing acid secretion with H2-receptor antagonists facilitates healing. Chronic gastritis tends to occur in elderly individuals and cause thinning and degeneration (atrophy) of the gastric mucosa. Chronic gastritis is classified as type A (fundal) or type B (antral), depending on the pathogenesis and location of the lesions. When both types of chronic gastritis occur, it is known as type AB or pangastritis, and the antrum (see attached pic) is more severely involved. Chronic fundal gastritis, also called atrophic or autoimmune gastritis, is the most severe type. The gastric mucosa degenerates extensively in the body and fundus of the stomach, leading to gastric atrophy. Loss of chief cells and partial cells diminishes acid secretion, so the feedback mechanism that normally inhibits gastrin secretion is impaired, causing elevated plasma levels of gastrin. Pernicious anemia (low RBC's) may develop because intrinsic factor is less available to facilitate vitamin B12 absorption in the ileum. A significant number of individuals with chronic fundal gastritis have antibodies to parietal cells, intrinsic factor, and gastric cells in their sera, suggesting that an autoimmune mechanism is involved in pathogenesis of the disease. The fact that chronic fundal gastritis occurs in association with other autoimmune diseases (e.g., rheumatoid arthritis, autoimmune thyroid disease, or type 1 diabetes mellitus) strengthens this association. Chronic fundal gastritis is a risk factor for gastric carcinoma, particularly in individuals who develop pernicious anemia. Chronic antral gastritis generally involves the antrum only and occurs more often than fundal gastritis. It is caused by H. pylori bacteria and it is also associated with use of alcohol, tobacco, and nonsteroidal anti-inflammatory drugs. There are high levels of hydrochloric acid secretion. H. pylori can also cause autoimmune atrophic gastritis and involve the fundus. In these cases there is greater risk for the development of gastric cancer. Signs and symptoms of chronic gastritis often include vague symptoms: anorexia, fullness, nausea, vomiting, and epigastic pain. Gastric bleeding may be the only clinical manifestation of gastritis. Gastroscopic examination and biopsy may show long-standing inflammatory process and gastric atrophy in an individual with no history of abdominal distress. Failure to stimulate acid secretion confirms acholorhydria (diminished secretion of hydrochloric acid). The gastric secretions also can be evaluated for the presence of intrinsic factor. Symptoms can usually be managed by eating smaller meals in conjunction with a soft, bland diet and by avoiding alcohol and aspirin. H. pylori infection is treated with antibiotics, and vitamin B12 is administered to correct pernicious anemia.
Postgastrectomy syndromes are a group of signs and symptoms that occur after gastric resection for the treatment of peptic ulcer, gastric carcinoma, or bariatric surgery for exterme obesity. They are caused by anatomic and functional changes in the stomach and upper small intestine and include the following:
1. Dumping syndrome: Rapid emptying of hypertonic chyme from the surgically residual stomach (the stomach component remaining after surgical resection following gastric or bariatric surgery) into the small intestine 10 to 20 minutes after eating; promoted by loss of gastric capacity, loss of emptying control when the pylorus is removed, and loss of feedback control of the duodenum when it is remove; responds to dietary management. Symptoms include cramping pain, nausea, vomiting, osmotic diarrhea, weakness, pallor, and hypotension.
2. Alkaline reflux gastritis: Stomach inflammation caused by reflux of bile and alkaline pancreatic secretions containing proteolyic enzymes that disrupt the mucosal barrier in the remnant stomach. Symptoms include nausea, bilious vomitting, and sustained epigastric pain that worsens after eating and is not relieved by antacids; responds somewhat to avoidance of aspirin and alcohol, but surgical correction may be required.
3. Afferent loop obstruction: Intermittent severe pain and epigastric fullness after eating as a result of volvulus, hernia, adhesion, or stenosis of the duodenal stump on the proximal side of the gastojejunostomy; vomiting relieves symptoms; management includes low-fat diet, but surgery is required for complete obstruction.
4. Diarrhea: either frequent, persistant elimination of liquid stool or intermittent, precipitous, and unpredictable elimination of a large volume of stool; related to rapid gastric emptying and osmotic attraction of water into the gut, especially after large intake of high-carbohydrate liquids; small, dry meals and anticholinergic drugs are effective control measures.
5. Weight loss: Commonly caused by inadequate caloric intake because individual cannot tolerate carbohydrates or a normal-size meal; stomach is also less able to mix, churn, and break down food. In the case of bariatric surgery for extreme obesity, weight loss is the intended outcome.
6. Anemia: Iron malabsorption may result from decreased acid secretion or lack of duodenum after Billroth II procedure (gastro-jejunostomy); deficiencies of iron and vitamin B12 or folate may result.
7. Bone amd mineral disorders: Related to altered calcium absorption and metabolism with increased risk for fractures and deformity and malabsorption of vitamins and nutrients, such as vitamin D.
pancreatic insufficiency: The pancreatic enzymes (lipase, amylase, typsin, chymotrypsin) are required for the digestion of proteins, carbohydrates, and fats. Pancreatic insufficiency is the deficient production of these enzymes, particularly lipase, by the pancreas. Causes include chronic pancreatitis, pancreatic carcinoma, pancreatic resection, and cystic fibrosis. Significant damage to or loss of pancreatic tissue must occur before enzyme levels decrease sufficiently to cause maldigestion. Although pancreatic insufficiency causes poor digestion of all nutrients, fat maldigestion is the chief problem. Absence of pancreatic bicarbonate in the duodenum and jejunum causes an acidic pH that worsens maldigestion by precipitating bile salts and preventing activation of the pancreatic enzymes that are present. A large amount of fat in the stool (steatorrhea) is the most common sign of pancreatic insufficiency. There is also a deficit of fat-soluble vitamins (A, D, E, and K).

lactase deficiency: Deficiency of disaccharidase at the brush border of the small intestine is caused by a genetic deficit in which a single enzyme, usually lactase, is lacking. Lactase deficiency inhibits the breakdown of lactose (milk sugar) into monosaccharides and therefore prevents lactose digestion and absorption across the intestinal wall. Lactase deficiency is most common in blacks, latinos, and Native Americans and usually does not develop until adulthood. Secondary (acquired) lactase deficiency can be caused by several diseases of the intestine, including glutensensitive enteropathy, enteritis, and bacterial overgrowth. The undigested lactose remains in the intestine, where bacterial fermentation causes gasses to form. Undigested lactose also increases the osmotic gradient in the intestine, causing irritation and osmotic diarhea. Clinical manifestations of lactose consumption with lactase deficiency are bloating, crampy pain, diarrhea, and flatulence. The disorder is diagnosed by a lactose-tolerance test. Avoiding more than 1 cup of milk per day and adhering to a lactose-free diet relieves symptoms.

bile salt deficiency: Conjugated bile acids (bile salts) are necessary for the digestion and absorption of fats. Bile salts are conjugated in the bile that is secreted from the liver. When bile enters the duodenum, the bile salts aggregate with fatty acids and monoglycerides to form micells. Micelle formation makes fat molecules more soluble and allows them to pass through the unstirred layer at the brush border of the small intestinal villi. A minimum concentration of bile salts, termed the critical micelle concentration, is required to allow micells to form. Therefore, conditions that decrease the production or secretion of bile result in decreased micelle formation and fat malabsorption. These conditions include advanced liver disease, which decreases the production of bile salts; obstruction of the common bile duct, which decreases the production of bile salts; obstruction of the common bile duct, which decreases flow of bile into the duodenum (cholestasis); intestinal stasis (lack of motility), which permits overgrowth of intestinal bacteria that deconjugate bile salts; and disease of the ileum, which prevent the reabsorption and recycling of bile salts (enterohepatic circulation). Clinical manifestations of bile salt deficiency are related to poor intestinal absorption of fat and fat-soluble vitamins (A, D, E, K). Increased fat in the stools (steatorrhea) leads to diarrhea and decreased plasma proteins. The losses of fat-soluble vitamins and their effects include the following:
1. Vitamin A deficiency results in night blindness.
2. Vitamin D deficiency results in decreased calcium absorption with bone demineralization (osteoporosis), bone pain, and fractures.
3. Vitamin K deficiency prolongs prothrombin time, leading to spontaneous development of purpura (bruising) and petechiae.
4. Vitamin E deficiency has uncertain effects but may cause testicular atrophy and neurologic defects in children.
The most effective treatment for fat-soluble vitamin deficiency is to increase medium-chain triglycerides in the diet, for example, by using coconut oil for cooking. Vitamins A, D, and K are given parenterally. Oral bile salts are an effective therapy.
ulcerative colitis: is a chronic inflammatory disease that causes ulceration of the colonic mucosa, most commonly in the rectum and sigmoid colon. The lesions appear in susceptible individuals between 20 and 40 years of age. Risk factors include family history of disease and jewish descent, and the disease is more prevalent among white populations. The familial tendency to develop UC and the occurrence of disease in identical twins support a genetic theory of causication. Perhaps most significant are humoral immunologic factors (Th2 response) and activated macrophages associated with the disease. Lymphocytes (T cells) in individuals with UC may have cytotoxic effects on the epithelial cells of the colon. Furthermore, autoimmune disorders, such as systemic lupus erythymatosus and erythrma nodsum, may accompany UC.

Crohn Disease: is an inflammatory disorder that affects both the large and small intestine. In a small percentage of cases, CD is difficult to differentiate from ulcerative colitis (table 34-6), however, the rectum is seldom ivolved. Risk factors and theories of causation are the same as those for ulcerative colitis, including genetic perdisposition and an altered immune response to intestinal bacteria. Of affected individuals, 10% to 20% have a positive family history. Increased activity of suppressor T cells, alterations in immunoglobulin A (IgA) production, activation of macrophages, and the presence of antibodies against luminal antigens, luminal flora, and susceptibility genes are factors associated with CD.
Diverticulitis:
Diverticula are herniations or saclike outpouchings of the mucosa and submucosa through the muscle layers, usually in the wall of the sigmoid colon. Diverticulosis is asymptomatic diverticular disease. Diverticulitis represents inflamation. Diverticular disease is most common among elderly women, but the incidence is increasing in younger individuals, particularly when much of the diet consists of refined foods.

Patho: Diverticula can occur anywhere in the gastrointestinal tract, and the most common sites are the left sigmoid colon in Western countries and the right colon in Asian countries. The exact etiology of diverticular disease remains unknown. The diverticula form from increases in intraluminal pressure, particularly at weak points in the colon wall, usually where arteries penetrate the tunica muscularis. A common associated finding is thickening of the circular muscles and shortening of the longitudinal (teniae coli) muscles surrounding the diverticula. Increased collagen and elastin deposition, not muscle hypertrophy, is associated with muscle thickening and this contributes to increased intraluminal pressure and herniation. Habitual consumption of a low-residue diet reduces fecal bulk, thus reducing the diameter of the colon. According to the law of lapace, wall pressure increases as the diameter of a cylindrical structure decreases. Therefore, pressure within the narrow lumen can increase enough to rupture the diverticula, causing inflammation and diverticulitis. Bacteria and local ischemia also may be contributing factors. Diverticulitis can rarely cause fistula, abscess formation, perforation, bowel obstruction, and peritonitis.

Clinical manifestations: Symptoms of diverticular disease may be vague or absent. Cramping pain of the lower abdomen can accompany constriction of the thickened colonic muscles. Diarrhea, constipation, distention, or flatulence may occur. If the diverticula become inflamed or abcesses form, the individual develops fever, leukocytosis (increased white blood cell count), and tenderness of the lower left quadrant.

Evaluations and treatment: Diverticula are often discovered during diagnostic procedures performed for other problems. Sigmoidoscopy or colonoscopy permits direct observation of the lesions. Abdominal computed tomography is used for diagnosis of diverticulitis. An increase of dietary fiber intake often relieves symptoms and probiotics and mesalazine are being evaluated. Uncomplicated diverticulitis is usually treated with nonabsorbable antibiotics, bowel rest, and analgesia. Laproscopic resection and other minimally invasive approaches are being implemented for more severe complications.

Appendicitis: is an inflammation of the vermiform appendix, which is a projection from the apex of the cecum (see attached pic). It is the most common surgical emergency of the abdomen and affects 7% to 12% of the population. It generally occurs between 20 and 30 years of age, although it may develop at any age.

Patho: The exact mechanism of the cause of appendicitis is controversial. Obstruction of the lumen with stool, tumors, or foreign bodies with consequent bacterial infection is the most common theory. The obstucted lumen does not allow drainage of the appendix, and as mucosal secretion continues, intraluminal pressure increases. The increased pressure decreases mucosal blood flow, and the appendix becomes hypoxic. The mucosa ulcerates, promoting bacterial or other microbial invasion with further inflammation and edema. Inflammation may involve the distal or entire appendix. Gangrene develops from thrombosis of the luminal blood vessels, followed by perforation.

Clinical manifestations: Gastric or periumbilical pain is the typical symptom of an inflamed appendix. The pain may be vague at first, increasing in intensity over 3 to 4 hours. It may be subside and then recur in the right lower quadrant, indicating extension of the inflammation to the surrounding tissues. Nausea, vomiting, and anorexia follow the onset of pain, and a low-grade fever is common. Diarrhea occurs in some individuals, particularly children; others have a sensation of constipation. Perforation, peritonitis, and abcess formation are the most serious complications of appendicitis.

Evaluation and treatment: In addition to clinical manifestations, the clinician can usually locate the painful site with one finger. Rebound tenderness is usually referred to the right lower quadrant. The white blood cell count ranges from 10,000 to 16,000 cells/mm with increased neutrophils. Ultrasonography and computed tomography (CT) scans can assist in differentiating appendicitis from perforated ulcer or cholecystis. Laparoscopic appendectomy is the treatment for simple or perforated appendicitis. Surgery provides quick recovery for simple appendicitis. Recovery is more compicated in cases of perforation or abscess formation.

Irritable bowel syndrome (IBS):
IBS is a functional gastrointestinal disorder with no specific structural or biochemical alterations as a cause of disease. It is broadly characterized by recurrent abdominal pain and discomfort associated with altered bowel habits that present as diarrhea or constipation or both. About 7% to 20% of the worlds population is estimated to have the disorder, and it is more common in women with a higher prevalence during youth and middle age. Individuals with symptoms of IBS are also more likely to have anxiety, depression, and chronic fatigue syndrome. Symptoms of IBS can negatively affect quality of life and activity and present a significant economic burden.

Patho: The pathophysiology of IBS is complex, but there is increasing evidence for organic disease. Several mechanisms are proposed to explain the causes for the symptoms listed here.
1. Visceral hypersensitivity or hyperalgesia particularly with distension of the rectum, but also other areas of the gut, may originate in either the peripheral or the central nervous system. The mechanism may be related to dysregulation of the "brain-gut axis" (alterations in gut or central nervous system processing of gut nociceptive information), changes in the role of serotonin in the enteric nervous system of the gut, activation of the gut immune system, or alterations in the autonomic nervous system.
2. Abnormal gastrointestinal motility and secretion are associated with IBS. Individuals with diarrhea-type IBS have more rapid colonic transmit times, whereas those with bloating and constipation have delayed transit times. The mechanism may also be related to visceral hypersensitivity as well as dysregulation of the brain-gut axis or alterations in the role of serotonin in the function of the entire nervous system.
3. Intestinal infection (bacterial enteritis) has been associated with symptoms of IBS, and postinfectious IBS appears to be related to ongoing low-grade inflammation, changes in intestinal permeability, and an abnormal immune response in gut tissues.
4. Overgrowth of small intestinal flora (normal gut bacteria) may precipitate IBS symptoms, and it is proposed that methane gas may slow intestinal transit time, resulting in constipation and bloating.
5. Food allergy or food intolerance is associated with IBS. Food antigens of food borne pathogens may activate the mucosal immune system, alter intestinal flora, or mediate hypersesitivity reactions and IBS symptoms. Food elimination approaches are helpful in some cases.
6. Psychosocial factors, including emotional stress, influence brain-gut interactions and neuroendocrine, autonomic nervous system, and pain modulatory responses, contributing to the symptoms of IBS.

Clinical manifestations: IBS is characterized by lower abdominal pain or discomfort (box34-1) and can be diarrhea-predominant, constipation-predominant, or alternating diarrhea/constipation. Symptoms including gas, bloating, and nausea are usually relieved with defecation and do not interfere with sleep.

Evaluation and treatment: The diagnosis of IBS is based on signs and symptoms and includes the exclusion of structural or biochemical causes of disease. Diagnostic procedures to rule out other causes of symptoms may include endoscopic evaluations, computed tomography (CT) scans or abdominal ultrasound, blood tests, and tests for lactose intolerance, celiac disease, or other disorders. The person may be evaluated for food allegies, parasites, or bacterial growth. The Rome III criteria for diagnosing IBS guides evaluation (LOOK AT BOX 34-1). There is no cure for IBS, and treatment is individualized. Pharmacologic treatment of symptoms may include laxatives and fiber, antidiarrheals, antispasmodics, low-dose antidepressants, visceral analgesics, and serotonin agonists or antagonists. Alternative therapies including probiotics, hypnosis, acupuncture, and psychotherapy are treatment options. Research continues to advance the management of this complex syndrome.

Vascular insufficiency:
Three branches of the abdominal aorta supply the stomach and intestines: the celiac axis (stomach, liver, spleen, pancreas), the superior mesenteric artery (small intestine arterial supply), and the inferior mescentric artery (large intestine arterial supply. Mescenteric arterial hypoperfusion is less common than occlusive lesions cause by atherosclerosis, thrombi, or emboli. Mesenteric vein thrombosis is the least common cause of mesenteric ischemia with symptoms similar to those for mesenteric arterial insufficiency but with a more prolonged course. Chronic mesenteric arterial insufficiency (hypoperfusion) is rare but can develop secondarily to congestive heart failure, acute myocardial infarction, hemorrhage, stenosis, thrombus formation, or any condition that decreases arterial blood flow. Elderly individuals with arteriosclerosis are particularly susceptible. Chronic occlusion is often accomplished by formation of collateral circulation. The collateral vessels may be able to nourish the resting intestine, but after eating, when the intestine requires more blood, the arterial supply may be insufficient. Ischemia develops, causing cramping abdominal pain (abdominal angina), a cardinal symptom. Some individuals suffer significant weight loss because they stop eating to control the pain. Progressive vascular obstruction eventually causes continuous abdominal pain and necrosis of the interstitial tissue. Acute mesenteric arterial insufficiency results from dissecting aortic aneurysms, ruptured aortic aneurysms (rare), or emboli. Embolic obstruction is associated with atrial fibrillation, mitral valve disease, and heart valve prosthesis. The superior mesenteric artery has a more direct line of flow from the aorta; therefore, emboli enter it more readily than the inferior branch, causing ischemia and necrosis of the small intestine. Initially, there is increased motility. Ischemia and necrosis (intestinal infarction) alter membrane permeability and the damaged intestinal mucosa cannot produce enough mucus to protect itself from digestive enzymes. Bloody diarrhea develops. Fluid moves from the blood vessels into the bowel wall and peritoneum, causing hypovolemia, and further decreases intestinal blood flow. As intestinal infarction progresses, abdominal pain is severe with a rigid distended abdomen, loss of bowel sounds, shock, peritonitis, leukocytosis, fever, and tachycardia. Diagnosis of mesenteric artery occlusion is based on clinical manifestations, mesenteric artery angiography, and abdominal imaging. Often a bruit can be heard over the occluded artery. Treatment includes aggressive rehydration and the use of antibiotics, anticoagulants, vasodilators, and inhibitors of reperfusion injury. Revascularization surgery is performed for both chronic and acute mesenteric arterial insufficiency when necrosis and infarction are suspected. Mortality is high for individuals with accute occlusion, compromised cardiac output, coexisting systemic disease, or delayed diagnosis.
Obesity is an increase in body fat mass and a metabolic disorder that has become an epidemic worldwide. The incidence is rapidly increasing among children and adolescents and they tend to become obese adults. Obesity is defined as a body mass index (BMI=kg/m2) that exceeds 30 and generally develops when caloric intake exceeds caloric expenditure. Obesity is a major risk factor for morbidity, death, and increased healthcare costs. Three leading causes of death associated with obesity are coronary artery disease, type 2 diabetes mellitus, and cancer (colon, breast in postmenopausal women, endometrial, prostate, kidney, and esophagus). Obesity also is a risk factor for hypertension, stroke, hepatobiliary disease (gallstones and nonalcoholic steatohepatitis), osteoarthritis, and infectious disease. Pulmonary function can be compromised by a large amount of adipose tissue overlying the chest cage, and obstructive sleep apnea syndrome can occur as a consequence. The causes and consequences of obesity are multiple and complex. Rapid advancing research regarding risk factors, casual mechanisms, and complications is in progress. Obesity is known to occur in families and genotypes, and gene-environment interactions are important predisoping factors. Environmental factors include culture, socioeconomic status, food intake status, and physical activity. Metabolic abnormalities associated with obesity include Cushing syndrome, Cushing disease, polycystic ovarian syndrome, hypothyroidism, and hypothalmic injury.

Patho: The patho of obesity is complex and involve s the interaction of numerous cytokines, hormones, and neurotransmitters. When adipocytes (fat cells) increase in size and number they secret hormones and cytokines, known as adipocytokines. The adipocytokines and other hormones participate in regulation of food intake, lipid storage, insulin sensitivity, vascular homeostasis, blood pressure regulation, angiogenesis, inflammatory and immune responses, female reproduction, and regulation of energy metabolism. Visceral fat accumulation causes dysfunction in the regulation and interaction of these cytokines and hormones and contributes to the complications and consequences of obesity. Neuroendocrine regulation of appetite, eating behavior, energy metablolism, and body fat mass is controlled by a dynamic circuit of signaling molecules from the periphery acting on the hypothalamus. The sources include insulin from the beta cells of the pancreas; ghrelin from the stomach; peptide YY from the intestines; and leptin, adiponectin, and resistin from adipose tissue. These hormones circulate in the blood at concentrations proportional to body fat mass and serve as peripheral signals to the hypothalamus, where appetite and metabolism are regulated. Obesity is associated with increased circulating plasma levels of leptin, insulin, resistin and ghrelin. There are decreased levels of adiponectin and peptide YY. Interaction of these altered levels of hormones and adipocytokines with neuropeptides at the level of the hypothalamus may be an important determinant of excessive fat mass and the complications of obesity. Leptin, adiponectin, and insulin resistance and also inflammation are particularly important in the complications of obesity. Leptin, a product of the obesity gene and expressed primarily by adipocytes, acts on the hypothalamus to suppress appetite and functions to regulate body weight within a fairly narrow range. Leptin levels increase as the number of adipocytes increase; however, for unknown reasons, high leptin levels are ineffective at decreasing appetite and energy expenditure, a condition known as leptin resistance. Leptin resistance disrupts hypothalmic satiety signaling and promotes overeating and excessive weight gain and is a factor in the development of obesity. Leptin resistance is also associated with insulin resistance (hyperinsulinemia/ glucose intolerance) and the cardiovascular complications of obesity. Obesity promotes a low-grade systemic inflammation that is related to T lymphocyte and macrophage infiltration of adipocytes with release of proinflammatory mediators. The inflammatory state and accelerated lipolysis contribute to the development of insulin resistance and metabolic syndrome (dyslipidemia, atherosclerosis, hypertension, cardiovascular disease, and type 2 diabetes mellitus). Decrease in the level of adiponectin, produced primarily by visceral adipose tissue, is associated with insulin resistance, coronary artery disease, and hypertension, contributing to the complications of obesity. Fig 34-10 summarizes the pathophysiology and major consequences of obesity.

Clinical manifestations: Obesity usually presents with two different forms of adipose tissue distribution. Visceral obesity (aka intra-abdominal, central, or masculine obesity) occurs when the distribution of body fat is localized around the abdomen and upper body, resulting in an apple shape. Visceral obesity has an increased risk for systemic inflammation, dyslipidemia, and insulin resistance with predisposition to atherosclerosis, hypertension, cardiovascular disease, cancer, and type 2 diabetes mellitus. This combination of traits is also known as metabolic syndrome. The dyslipidemia (Abnormally elevated cholesterol or fats (lipids) in the blood) of obesity is associated with accelerated lipolysis, particularly from visceral fat, with the elevation in levels of plasma nonesterified fatty acids, triglycerides, and low-density lipoprotein and the reduction in levels of high-density lipoprotein increasing the risk for atherosclerosis and cardiovascular disease. Peripheral obesity (aka as gluteal-femoral or feminine obesity) occurs when the distribution of body fat is extraperitoneal and distributed around the thighs and buttocks, resulting in a pearsheap, and is more common in women. Subcutaneous fat is more generally distributed over the body. Peripheral and subcutaneous fat is less metabolically active, is less lipolytic, and releases less adipocytokines (particularly adiponectin) than visceral fat. Risk factors are still present for the complications of obesity but they are less severe than those for visceral obesity.

Evaluation and treatment: There are several methods for measuring or estimating body fat mass, including computed tomography (CT) and magnetic resonance imaging (MRI) techniques; bioimpedence analysis; underwater weighing; and anthropometric measurements, such as skinfold thickness, circumferences, and various body diameters (e.g., waste-to-hip ratios and waist circumference; body mass index tables). The BMI and waiste-to-hip ratios are most commonly used because they are easiest to measure, and waist measurements are associted with increases in viceral fat. Overweight is defined as a BMI greater than 25 and obesity is a BMI greater than 30. BMI charts are available for children ages 2 to 20 years; these can be used for comparison during adulthood because obese children generally become obese adults. No specific diagnostic criteria for obesity have been established. The complications of obesity affect nearly every body system. Obesity is a chronic disease for which various approaches to treatment have been used; these include correction of metabolic abnormalities, individually tailored weight reduction diets and exercise programs, psychotherapy, behavioral modification, medications, and weight loss (bariatric) surgery. Unraveling the causes of obesity will lead to more specific prevention and pharmacotherapeutic strategies.
Short-term:
aka extended fasting, consists of several days of total dietary abstinence or deprivation. Once all available energy has been absorbed from the intestine, glycogen in the liver is converted to glucose through glycogenolysis, the metabolism of glycogen into glucose. This process peaks within 4 to 8 hrs, and gluconeogenesis begins. Gluconeogenesis is the formation of glucose from noncarbohydrate molecules: lactate, pyruvate, amino acids, and the glycerol portion of fats. Like glycogenolysis, gluconeogenesis takes place within the liver. Both of these processes deplete stored nutrients and thus cannot meet the body's energy needs indefinitely. Proteins continue to be catabolized to a minimal degree, providing carbon for the synthesis of glucose. The kidney converts glutamine to glucose, significantly contributing to glucose production. Fatigue decreases physical activity and energy expenditure.

Long term:
begins after several days of dietary abstinence and eventually causes death. The major characteristic of long-term starvation is a decreased dependence on gluconeogenesis and an increased use of ketone bodies (products of lipid and pyruvate metabolism) as a cellular energy source. Depressed insulin and glucagon levels promote lipolysis in adipose tissue. Lipolysis liberates fatty acids, which supply energy to cardiac and skeletal muscle cells, as well as ketone bodies, which sustain brain tissue. Fatty acid or ketone body oxidation meets most energy needs of the cells. (some glucose is still needed as fuel for brain tissue.) Once the supply of adipose tissue is depleted, protolysis begins. The breakdown of muscle protein is the last process to supply energy for life. Death results from severe alterations in electrolyte balance and loss of renal, pulmonary, and cardiac function. Adequate ingestion of appropriate nutrients is the obvious treatment for starvation. In medically induced starvation, the body is maintained in a ketotic state until the desired amount of adipose tissue has been lysed. Starvation imposed by chronic disease, long-term illness, or metabolism is treated with enteral or parenteral nutrition.
-Portal hypertension: is abnormally high blood pressure in the portal venous system (aka liver venous system). Pressure in this system is normally 3 mm Hg; portal hypertension is an increase to at least 10 mm Hg.

-Ascites: is the accumulation of fluid in the peritoneal cavity (two membanes that seperate the organs in the abdominal cavity). Ascites traps body fluid in a "third space" (a space where it does not normally collect) from which it cannot escape. The effect is to reduce the amount of fluid available for normal physiologic functions. Cirrhosis is the most common cause of ascites, but other causes include heart failure, constrictive pericarditis, abdominal malignancies, nephrotic syndrome, and malnutrition. Of individuals who develop ascites caused by cirrhosis, 25% die within 1 year. Continued heavy drinking of alcohol is associated with this mortality.

-hepatic encephalopathy (portal-systemic encephalopathy) is a complex neurologic syndrome characterized by impaired cerebral function, flapping tremor (asterixis), and electroencephalogram (EEG) changes. The syndrome may develop rapidly during acute fulminant hepatitis or slowly during chronic liver disease and the development of portal hypertension.

-Jaundice, or icterus, is a yellow or greenish pigmentation of the skin caused by hyperbilirubinemia (plasma bilirubin [breakdown products of RBC's] concentrations greater than 2.5 to 3.0 mg/dl). Hyperbilirubinemia and jaundice can result from (1) extrahepatic (posthepatic) obstruction to bile flow, (2) intrahepatic obstruction, or (3) prehepatic excessive production of unconjugated (blended) bilirubin (i.e. excessive hemolysis of red blood cells) (LOOK at fig 34-14). Jaundice in newborns is caused by impaired bilirubin uptake and conjugation.
Viral Hepatitis patho: All five types of viral hepatitis (A, B, C, D and E) can cause acute, icteric illness. The pathologic lesions of hepatitis include hepatic cell necrosis, scarring (with chronic disease), and Kupffer cell hyperplasia. Infiltration by mononuclear phagocytes occurs with varying severity. Regeneration of hepatic cells begins within 48 hours of injury. The inflammatory process can damage and obstruct bile canaliculi, leading to cholestasis and obstructive jaundice. In milder cases, the liver parenchyma is not damaged. Damage tends to be most severe in cases of hepatitis B and C. Hepatitis B is also associated with acute fulminating hepatitis, a rare form of the disease that is characterized by massive hepatic necrosis. Acute fulminating hepatitis causes sever encephalopathy, which is manifested as confusion, stupor, and coma. Liver failure can occur, leading to intestinal bleeding, cardiorespiratory insufficiency, and renal failure. Co-infection of hepatitis B virus (HBV), hepatitis C virus (HCV), hepatitis D virus (HDV), and human immunodeficiency virus (HIV) occurs because these viruses share the same route of transmission (contact between infected body fluids and broken skin or mucous membranes or intavenously). Progression of liver disease is more rapid in these cases.

Fulminant Viral Hepatitis Patho:
Fulminant viral hepatits causing acute liver failure (fulminant liver failure) is a clinical syndrome resulting in severe impairment or necrosis of liver cells and potential liver failure. The disorder rarely occurs with HAV and may occur as a complication of hepatitis C or hepatitis B, particularly HBV infection compounded by infection with the delta virus. Toxic reactions to drugs and congenital metabolic disorders also can cause fulminant hepatitis. Acetaminophen overdose is the leading cause of acute liver failure in the United States. Edematous hepatocytes and patchy areas of necrosis and inflammatory cell infiltrates disrupt the parenchyma. The death of hepatocytes may be caused by viral or immunologic damage.
Alcoholic cirrhosis:
Cause: Caused by the toxic affects of alcohol metabolism on the liver, immunologic alterations, inflammatory cytokines, oxidative stress from lipid peroxidation, and malnutrition. Alcohol is transformed to acetalehyde, and excessive amounts significantly alter hepatocyte function and activate hepatic stellate cells, a primary cell involved in liver fibrosis. Mitochondrial function is impaired decreasing oxidation of fatty acid. Enzyme and protein synthesis may be depressed or altered, and ammonia degranulation is diminished. Acetaldehyde inhibits export of protein from the liver, alters metabolism of vitamins and minerals, and induces malnutrition. Cellular damage initiates an inflammatory response that, along with necrosis, results in excessive collagen formation. Fibrosis and scarring alter the structure of the liver and obstruct biliary and vascular channels.

Treatment: No specific treatment for alcoholic steatohepatitis or cirrhosis. Rest, vitamin supplements, a nutritious diet, and management of complications, such as ascites, gastrointestinal bleeding and encephalopathy are essential. Cessation if drinking is essential and slows the progression of liver damage, improves clinical symptoms, and prolongs life. Individuals with severe symptoms are treated with a regimen of corticosteroids.

Prognosis: Death

Biliary cirrhosis:

Cause: Differs from alcoholic cirrhosis in that the damage and inflammation leading to cirrhosis begin in bile canaliculi and bile ducts, rather than in the hepatocytes. The two types of biliary cirrhosis are primary and secondary. Although both involve bile duct pathologic changes, they differ with respect to cause, risk factors, and mechanisms of obstruction and inflammation as follows:
1. Primary biliary cirrhosis:
-Caused by autoimmune T lymphocyte and antibody-mediated destruction of the small intrahepatic bile ducts.
-Treatment with ursodeoxycholic acid slows disease progression and liver transplant is highly effective
-Life expectancy w/o treatment is 5-10 years after onset of symptoms

2. Secondary biliary cirrhosis:
-Caused by prolonged partial or complete obstruction of the common bile duct or branches by gallstones, tumors, fibrotic strictures, or chronic pancreatitis
-surgery or endoscopy relieves obstruction, prolongs survival, and diminishes or resolves symptoms
-prognosis good following surgery
Cholelithiasis (gallstones) patho:
Gallstones are commonly of two types: cholesterol (most common) and pigmented. Cholesterol gallstones form in bile that is supersaturated with cholesterol produced by the liver. Supersaturation sets the stage for cholesterol crystal formation, or the formation of "microstones." More crystals then aggregate on the microstones, which grow to form "macrostones." This process usually occurs in the gallbladder, which may have decreased motility. The stones can accumulate and fill the entire gallbladder. Pigmented stones form from increased levels of unconjugated bilitubin, which binds with calcium. They are associated with chronic liver disease.

Cholecystitis Patho:
Can be acute or chronic, but both forms are almost always caused b a gallstone lodged in the cysitic duct. Acute acalculous cholecystitis has been reported as a compication of surgery, multiple trauma or burn injury is treated with cholecystostomy. The gallbladder becomes distended and inflamed, with pain similar to that caused by gallstones. Pressure against the distended wall of the gallbladder decreases blood flow and may result in ischemia, necrosis, and perforation. Fever, leukocytosis, Rebound tenderness and abdominal muscle guarding are common findings. Serum bilirubin and alkaline phosphate levels may be elevated. The acute abdominal pain of cholecystitis must be differentiated from that caused by pancreatitis, myocardial infarction, and acute pyelonephritis of the right kidney.
Acute Pancreatitis: is usually a mild disease (edematous pancreatitis) and resolves spontaneously, but about 20% of those with the disease develop a severe acute (necrotizing or hemorrhagic) pancreatitis requiring hospitalization. Pancreatitis develops because of obstruction to the outflow of pancreatic digestive enzymes caused by bile and pancreatic duct obstruction (e.g., gallstones). The obstructed ducts result in accumulation of pancreatic secretions and pathologic activation of enzymes (activated tryosin activities chymotrypsin, lipase, and elastase) with the pancreas. The activated intracellular enzymes cause autodigestion of pancreatic cells and tissues, resulting in inflammation and acute pancreatitis. The autodigestion causes vascular damage, coagulation necrosis, fat necrosis (see Ch. 3), and edema within the pancreas.

Chronic Pancreatitis: Irreversible structural or functional impairment of the pancreas leads to chronic pancreatitis. Chronic alcohol abuse is the most common cause; smoking and genetic factors increase the risk of chronic pancreatitis. Chronic exposure to toxic metabolites and release of proinflammatory cytokines contribute to cellular destruction including acinar cells and cells in the islets of Langerhans. Fibrosis, strictures, calcification, ductal obstruction, and pancreatic cysts are the common lesions of chronic pancreatitis. The cysts are walled-off areas or pockets of pancreatic juice, necrotic debris, or blood within or adjacent to the pancreas.