Digestivo II Past Paper PDF

DIGESTIVO II Esophageal atresia and tracheoesophageal fistula ▪ Discovered shortly after birth, usually due to regurgitation during feeding. ▪ In esophageal atresia a thin, noncanalized cord replaces a segment of esophagus, causing a mechanical obstruction. ▪ Atresia occurs mo...

DIGESTIVO II Esophageal atresia and tracheoesophageal fistula ▪ Discovered shortly after birth, usually due to regurgitation during feeding. ▪ In esophageal atresia a thin, noncanalized cord replaces a segment of esophagus, causing a mechanical obstruction. ▪ Atresia occurs most commonly at or near the tracheal bifurcation and is usually associated with a fistula connecting the upper or lower esophageal pouches to a bronchus or the trachea. ▪ In other cases, a fistula can be present without atresia. ▪ Either form of fistula can lead to aspiration, suffocation, pneumonia, and severe fluid and electrolyte imbalances. Diaphragmatic Hernia ▪ Diaphragmatic hernia occurs when no ciera bien el esphincter : el intestino sube incomplete formation of the diaphragm allows the abdominal viscera to herniate into the thoracic cavity. ▪ When severe, the space-filling effect of the displaced viscera can cause pulmonary hypoplasia that is incompatible with life. Omphalocele Gastroschisis no se ciera bien la pared cutanea ; intestino a fuera ◦ Closure of the abdominal musculature is ◦ Similar to omphalocele except that it incomplete and the abdominal viscera involves all of the layers of the abdominal herniate into a ventral membranous sac. wall, from the peritoneum to the skin.  Meckel Diverticulum parte del intestino parecido al ▪ A true diverticulum is a blind outpouching of the alimentary tract that communicates with the lumen and includes all three layers of the bowel wall. ▪ The most common true diverticulum is the Meckel diverticulum, which occurs in the ileum. ▪ Meckel diverticulum occurs as a result of failed involution of the vitelline duct, which connects the lumen of the developing gut to the yolk sac. ▪ This solitary diverticulum extends from the antimesenteric side of the bowel. ▪ The “rule of 2s” : Occur in approximately 2% of the population Are generally present within 2 feet (60 cm) of the ileocecal valve Are approximately 2 inches (5 cm) long Are twice as common in males Are most often symptomatic by age 2 (only approximately 4% are ever symptomatic). Pyloric Stenosis estrecho pyloro = vomita porque el contenido no puedo pasar se dilata el final del colon (descendente) : megacolon no tienes ganglios Hirschsprung Disease ◦ Hirschsprung disease occurs in approximately 1 of 5000 live births. ◦ Also known as congenital aganglionic megacolon. ◦ Results when the normal migration of neural crest cells from cecum to rectum is arrested prematurely or when the ganglion cells undergo premature death. ◦ This produces a distal intestinal segment that lacks both the Meissner submucosal and the Auerbach myenteric plexus (“aganglionosis”). ◦ Coordinated peristaltic contractions are absent and functional obstruction occurs, resulting in dilation proximal to the affected segment. ◦ Morphology: ◦ Diagnosis of Hirschsprung disease requires documenting the absence of ganglion cells within the affected segment. ◦ In addition to their characteristic morphology in hematoxylin and eosin– stained sections, ganglion cells can be identified using immunohistochemical stains for acetylcholinesterase. Achalasia estrecha : comida no puede passar ▪ Increased tone of the lower estophago se dilata esophageal sphincter (LES), as a result of impaired smooth muscle dolor relaxation, is an important cause of esophageal obstruction. ▪ Achalasia is characterized by the triad of incomplete LES relaxation, increased LES tone, and aperistalsis of the esophagus. ▪ Symptoms include dysphagia for solids and liquids, difficulty in belching, and chest pain. ▪ Secondary achalasia may arise in Chagas disease, in which Trypanosoma cruzi infection causes destruction of the myenteric plexus, failure of peristalsis, and esophageal dilatation. ▪ Treatment modalities for both primary and secondary achalasia aim to overcome the mechanical obstruction, and include laparoscopic myotomy and pneumatic balloon dilatation. Mallory-Weiss syndrome frecuente ; cuando una persona vomita mucho (anorexia ; alcohol) = laceracion del esophago = vomito sangre tambien (reversible : deja de vomitar con omeprazol) ▪ Longitudinal mucosal tears near the no congenital gastroesophageal junction. ▪ Associated with severe retching or vomiting secondary to acute alcohol intoxication. vomita sangre :  reflejo : no ciera bien el esphincter Reflux Esophagitis irritation del esophago esophago de = metaplasia transformation del epithelio del esophago ▪ The stratified squamous epithelium of the esophagus is resistant to abrasion from foods but is sensitive to acid. ▪ Submucosal glands, which are most abundant in the proximal and distal esophagus, contribute to mucosal protection by secreting mucin and bicarbonate. More importantly, the tone of the lower esophageal sphincter prevents reflux of acidic gastric contents, which are under positive pressure and would otherwise enter the esophagus. endoscopia ▪ Reflux of gastric contents into the lower esophagus is the most frequent cause of esophagitis. ▪ The associated clinical condition is termed gastroesophageal reflux disease (GERD). ▪ The most common cause of gastroesophageal reflux is transient lower esophageal sphincter relaxation. ▪ The most frequent clinical symptoms are heartburn, dysphagia, and regurgitation of sour-tasting gastric contents. Rarely, chronic GERD is punctuated by attacks of severe chest pain that may be mistaken for heart disease. Histology: ▪ Inflammatory cells in epithelial layer (eosinophils, neutrophils, excess T cells); ▪ Acanthosis and papillomatosis ▪ Basal cell hyperplasia ▪ Ballooned squamous cells ▪ Vascular ectasia in lamina propria scamoso = esophago glandular = estomago reflujo = cambia : epitelio glandular al final del esophago Esophageal Varices ▪ Venous blood from the GI tract passes through the liver, via the portal vein, before returning to the heart. This circulatory pattern is responsible for the first-pass effect in which drugs and other materials absorbed in the intestines are processed by the liver before entering the systemic circulation. Diseases that impede this flow cause portal hypertension and can lead to the development of esophageal varices, an important cause of esophageal bleeding. ▪ Portal hypertension results in the development of collateral channels at sites where the portal and caval systems communicate. ▪ These collateral veins allow some drainage to occur, but at the same time they lead to development of congested subepithelial and submucosal venous plexi within the distal esophagus and proximal stomach. These vessels, termed varices, develop in the vast majority of cirrhotic patients, most commonly in association with alcoholic liver disease. esophago con varices : vomita sangre hematemesis higado cirrhosis : metaplasia del epitelio gastro que invade al esophago Barrett Esophagus !!!!!!!!!!!!!!! cuando se produce una metaplasia del epitelio glandular a scamoso ▪ Barrett esophagus is a complication of en la union gastroesophagial chronic GERD that is characterized by intestinal metaplasia within the esophageal squamous mucosa. ▪ The incidence of Barrett esophagus is rising, and it is estimated to occur in as many as 10% of individuals with symptomatic GERD. ▪ The greatest concern in Barrett esophagus is that it confers an increased risk of esoph- ageal adenocarcinoma. ▪ The presence of dysplasia, a preinvasive change, is associated with prolonged symptoms, longer segment length, increased patient age, and Caucasian race.  Morphology zona roja irritada ▪ Barrett esophagus can be recognized as one or several tongues or patches of red, velvety mucosa extending upward from the gastroesophageal junction. ▪ This metaplastic mucosa alternates with residual smooth, pale squamous (esophageal) mucosa and interfaces with light-brown columnar (gastric) mucosa distally. ▪ The risk of dysplasia correlates with length of esophagus affected. metaplasia Histology ◦ Diagnosis of Barrett esophagus requires endoscopic evidence of metaplastic columnar mucosa above the gastroesophageal junction. ◦ Microscopically, intestinal-type metaplasia is seen as replacement of the squamous esophageal epithelium with goblet cells. cambios que pueden evolucionar a cancer ◦ When dysplasia is present, it is classified as low grade or high grade. Chronic Gastritis. Helicobacter pylori Gastritis produce gastritis and linfoma Morfology: H. pylori-infected antral mucosa is usually ▪ The most common cause of chronic gastritis is erythematous and has a coarse or even nodular infection with the bacillus H. pylori. appearance. The superficial lamina propria contains large ▪ H. pylori are spiral-shaped or curved bacilli present numbers of lymphocytes and plasma cells and in gastric biopsy specimens of almost all patients with the inflammatory infiltrate generally includes duodenal ulcers as well as most individuals with variable numbers of neutrophils with an gastric ulcers or chronic gastritis. intraepithelial location. ▪ Humans are the primary carriers, suggesting that Lymphoid aggregates, some with germinal transmission is primarily by the fecal-oral route. centers, are frequently present and represent an ▪ Infection is typically acquired in childhood and induced form of mucosa-associated lymphoid persists for life without treatment. tissue, or MALT, that has the potential to ▪ H. pylori infection most often presents as a transform into lymphoma. predominantly antral gastritis with normal or The organism is concentrated within the increased acid production. superficial mucus overlying epithelial cells in the surface and neck regions. ▪ Effective treatments for H. pylori infection include Organisms are most easily demonstrated with combinations of antibiotics and proton pump special stains: Warthin-Starry silver stain inhibitors  inflammacion y gastritis ; hemorrhagia digestiva + ulcer bacilli When inflammation remains limited to the antrum, increased acid production results in greater risk of duodenal peptic ulcer. In other patients gastritis may progress to involve the gastric body and fundus. This multifocal atrophic gastritis is associated with patchy mucosal atrophy, reduced parietal cell mass and acid secretion, intestinal metaplasia, and increased risk of gastric adenocarcinoma. Thus, there is an inverse relationship between duodenal ulcer and gastric adenocarcinoma that correlates with the pattern of gastritis Autoimmune Gastritis no infeccion ; autoimmune deterioran las cellulas del estomago no puede absorber nutrientes y vitamine B12 = anemia pernisiosa (no puede absorberla) Pathogenesis. ▪ Autoimmune gastritis accounts for less than 10% of The absence of acid production stimulates gastrin cases of chronic gastritis. release, resulting in hypergastrinemia and ▪ In contrast to H. pylori–associated gastritis, hyperplasia of antral gastrin-producing G cells. autoimmune gastritis typically spares the antrum Lack of intrinsic factor disables ileal vitamin and is associated with hypergastrinemia. B12 absorption, which ultimately leads to vitamin B12 deficiency and a slow-onset ▪ Autoimmune gastritis is characterized by: megaloblastic anemia (pernicious anemia) Antibodies to parietal cells and intrinsic factor that can be detected in serum and gastric secretions Reduced serum pepsinogen I concentration Endocrine cell hyperplasia Vitamin B12 deficiency Defective gastric acid secretion (achlorhydria) parietal cells ! metaplasia y adenocarcinoma possible metaplasia estomago que cambia al intestino  problema de mala absorpsion Mucosal Atrophy and Intestinal Metaplasia ◦ Long-standing chronic gastritis that involves the body and fundus may ultimately lead to significant loss of parietal cell mass. This oxyntic atrophy may be associated with intestinal metaplasia, recognized by the presence of goblet cells, and is strongly associated with increased risk of gastric adenocarcinoma. The risk of adenocarcinoma is greatest in autoimmune gastritis. This may be because achlorhydria of gastric mucosal atrophy permits overgrowth of bacteria that produce carcinogenic nitrosamines. Intestinal metaplasia also occurs in chronic H. pylori gastritis and may regress after clearance of the organism.  Intestinal Obstruction problema = el intestino se cierra = peitonitis Hernias Adhesions Volvulus Intussusception se sale de la pared se da la vuelta - ninos Any weakness or defect in the Surgical procedures, infection, or Twisting of a loop of bowel Intussusception occurs when a abdominal wall may permit protrusion other causes of peritoneal about its mesenteric point segment of the intestine, of a serosa-lined pouch of peritoneum inflammation, such as of attachment. constricted by a wave of called a hernia sac. endometriosis, may result in It results in both luminal peristalsis, telescopes into the development of adhesions and vascular compromise immediately distal segment. Hernias are the most frequent cause of between bowel segments It occurs most often in Untreated intussusception may intestinal obstruction worldwide. These fibrous bridges can create large redundant loops of progress to intestinal obstruction, closed loops through which other sigmoid colon compression of mesenteric Pressure at the neck of the pouch may viscera may slide and become vessels, and infarction. impair venous drainage of the entrapped, resulting in internal entrapped viscus. The resultant stasis herniation. Intussusception is the most and edema increase the bulk of the Sequelae, including obstruction common cause of intestinal herniated loop, leading to permanent and strangulation. obstruction in children younger entrapment (incarceration) and, over than 2 years of age. time, arterial and venous compromise (strangulation), and infarction peligroso : se perfore ; obstruction -> infecciones Ischemic Bowel Disease atherosclerosis : causa 1 de The severity of vascular compromise, the time frame ▪ The majority of the GI tract is supplied by the celiac, during which it develops, and the vessels affected superior mesenteric, and inferior mesenteric are the major variables in ischemic bowel disease. Two arteries. aspects of intestinal vascular anatomy also contribute ▪ Interconnections between arcades, as well as to the distribution of ischemic damage and are worthy collateral supplies from the proximal celiac and distal of note: pudendal and iliac circulations, make it possible for the small intestine and colon to tolerate slowly Intestinal segments at the end of their respective arterial progressive loss of blood supply from one artery. supplies are particularly susceptible to ischemia. These ▪ In contrast to chronic, progressive hypoperfusion, watershed zones include the splenic flexure, where the acute compromise of any major vessel can lead to superior and inferior mesenteric arterial circulations infarction of several meters of intestine. terminate, and, to a lesser extent, the sigmoid colon and rectum where inferior mesenteric, pudendal, and iliac ▪ Damage can range from mucosal infarction, extending arterial circulations end. Generalized hypotension or no deeper than the muscularis mucosae; to mural hypoxemia can therefore cause localized injury, and infarction of mucosa and submucosa; to transmural ischemic disease should be considered in the differential infarction involving all three wall layers. diagnosis of focal colitis of the splenic flexure or ▪ While mucosal or mural infarctions can follow acute rectosigmoid colon. or chronic hypoperfusion, transmural infarction is Intestinal capillaries run alongside the glands, from crypt to surface, before making a hairpin turn to empty into the typically caused by acute vascular obstruction. post-capillary venules. This arrangement makes the surface epithelium particularly vulnerable to ischemic injury, relative to the crypts. Histology ◦ Microscopic examination of ischemic intestine demonstrates the characteristic atrophy or sloughing of surface epithelium. ◦ In contrast, crypts may be hyperproliferative. ◦ Inflammatory infiltrates are initially absent in acute ischemia, but neutrophils are recruited within hours of reperfusion. Chronic ischemia is accompanied by fibrous scarring of the lamina propria and, uncommonly, stricture formation. In both acute and chronic ischemia, bacterial superinfection and enterotoxin release may induce pseudomembrane formation that resembles Clostridium difficile–associated pseudomembranous colitis. Malabsorption ▪ Malabsorption, which presents most commonly as chronic diarrhea, is characterized by defective absorption of fats, fat- and water-soluble vitamins, proteins, carbohydrates, electrolytes and minerals, and water. ▪ Chronic malabsorption can be accompanied by weight loss, anorexia, abdominal distention, borborygmi, and muscle wasting. ▪ A hallmark of malabsorption is steatorrhea, characterized by excessive fecal fat and bulky, frothy, greasy, yellow or clay-colored stools.  gluten : no puedes absorber Celiac Disease detection : ninos que no crecen , vomitos, diarrhea autoimmune ▪ Celiac disease is also known as celiac sprue or gluten-sensitive enteropathy. ▪ It is an immune-mediated enteropathy triggered by the ingestion of gluten-containing foods, such as wheat, rye, or barley, in genetically predisposed individuals.  se atrofia el epithelio intestinal : menos velocidades menos surperficie de absorption infiltrado linflammatorio mas denso lymphactico aumenta Morphology ◦ Biopsy specimens from the second portion of the duodenum or proximal jejunum, which are exposed to the highest concentrations of dietary gluten, are generally diagnostic in celiac disease. ◦ The histopathology is characterized by : ◦ -Increased numbers of intraepithelial CD8+ T lymphocytes (intraepithelial lymphocytosis). ◦ - Crypt hyperplasia ◦ -Villous atrophy ◦ - Increased numbers of plasma cells, mast cells, and eosinophils, especially within the upper part of the lamina propria.  infiltra inflammatorio muy denso y no velocidad 0 = normal la atrofia intestino = reversible 3C = peor pero celiaca a vida gradar una enfermedad celiaca se puede recuperar si no come gluten Infectious Enterocolitis ▪ Enterocolitis can present with a broad range of symptoms including diarrhea, abdominal pain, urgency, perianal discomfort, incontinence, and hemorrhage. ▪ Etiology varies with age, nutrition, and host immune status as well as environmental influences. diarrhea que afecta al epitelio Pseudomembranous Colitis intestino grueso ▪ Pseudomembranous colitis, generally caused by C. difficile, can also be referred to as antibiotic-associated colitis or antibiotic-associated diarrhea. ▪ It is likely that disruption of the normal colonic una infeccion por microbiota by antibiotics allows C. difficile claustridium difficile overgrowth. ▪ Fully developed C. difficile–associated colitis is oportunista : se associa a la toma accompanied by formation of de antibiotico pseudomembranes made up of an adherent layer of inflammatory cells and debris at sites of colonic mucosal injury. ▪ While pseudomembranes are not specific and may occur with ischemia or necrotizing infections, the histopathology of C. difficile- associated colitis is pathognomonic. ▪ The surface epithelium is denuded, and the superficial lamina propria contains a dense infiltrate of neutrophils and occasional fibrin thrombi within capillaries. Superficially damaged crypts are distended by a mucopurulent exudate that forms an eruption reminiscent of a volcano. These exudates coalesce to form pseudomembranes. Whipple Disease ◦ Whipple disease is a rare, multivisceral chronic disease first described as intestinal lipodystrophy in 1907 by George Hoyt Whipple. ◦ Whipple's original case report described an individual with malabsorption, lymphadenopathy, and arthritis of undefined origin. ◦ Postmortem examination demonstrated the presence of foamy macrophages and large numbers of argyrophilic rods in the lymph nodes, suggesting that the disease was caused by a microbe. The gram-positive actinomycete, named Tropheryma whippelii, which is responsible for Whipple disease, was identified by PCR in 1992 and finally cultured in 2000. ◦ Clinical symptoms occur because organism-laden macrophages accumulate within the small intestinal lamina propria and mesenteric lymph nodes, causing lymphatic obstruction. Thus, the malabsorptive diarrhea of Whipple disease is due to impaired lymphatic transport.  affecta a los lynfocitos y macrophagos Morphology ◦ The morphologic hallmark of Whipple disease is a dense accumulation of distended, foamy macrophages in the small intestinal lamina propria. ◦ The macrophages contain periodic acid–Schiff (PAS)-positive, diastase- resistant granules that represent lysosomes stuffed with partially digested bacteria. ◦ In Whipple disease, bacteria-laden macrophages can accumulate within mesenteric lymph nodes, synovial membranes of affected joints, cardiac valves, the brain, and other sites.  Crohn : alteracion immunologica no infeccion Inflammatory Bowel Disease ▪ Inflammatory bowel disease (IBD) is a chronic condition resulting from inappropriate mucosal immune activation. ▪ The two disorders that comprise IBD are ulcerative colitis and Crohn disease. ▪ The distinction between ulcerative colitis and Crohn disease is based, in large part, on the distribution of affected sites and the morphologic expression of disease. ▪ Ulcerative colitis is limited to the colon and rectum and extends only into the mucosa and submucosa. In contrast, Crohn disease, which has also been referred to as regional enteritis (because of frequent ileal involvement) may involve any area of the GI tract and is typically transmural. biopsia alteracion de la mucosa corticoides treatment  immunologica affecta a toda la pared del intestino Pathogenesis  Crohn Disease aphtas , ulceras , fissuras , pared estrecha Morphology alteration de la mucosa por la inflammacion ◦ Crohn disease may occur in any area of the GI tract, but the most common sites involved at presentation are the terminal ileum, ileocecal valve, and cecum. ◦ The presence of multiple, separate, sharply delineated areas of disease, resulting in skip lesions, is characteristic of Crohn disease and may help in the differentiation from ulcerative colitis. ▪ The earliest lesion, the aphthous ulcer, may progress, and multiple lesions often coalesce into elongated, serpentine ulcers oriented along the axis of the bowel. ▪ Edema and loss of the normal mucosal texture are common. ▪ Sparing of interspersed mucosa, a result of the patchy distribution of Crohn disease, results in a coarsely textured, cobblestone appearance in which diseased tissue is depressed below the level of normal mucosa ▪ Fissures frequently develop between mucosal folds and may extend deeply to become fistula tracts or sites of perforation ▪ The intestinal wall is thickened and rubbery as a consequence of transmural edema, inflammation, submucosal fibrosis, and hypertrophy of the muscularis propria, all of which contribute to stricture formation ▪ In cases with extensive transmural disease, mesenteric fat frequently extends around the serosal surface (creeping fat)  predisposition grados puede perforarse no congenital  Crohn : metaplasia y granulomas Histology autoimmunologica ▪ Clusters of neutrophils within a crypt are referred to as crypt abscesses, often associated with crypt destruction. ▪ Ulceration is common in Crohn disease, and there may be an abrupt transition between ulcerated and adjacent normal mucosa. ▪ Distortion of mucosal architecture ▪ Pseudopyloric metaplasia. ▪ Paneth cell metaplasia may also occur in the left colon, where Paneth cells are normally absent. ▪ Noncaseating granulomas, a hallmark of Crohn disease, are found in approximately 35% of cases and may occur in areas of active disease or uninvolved regions in any layer of the intestinal wall. Granulomas may also be present in mesenteric lymph nodes. ▪ Fissures ▪ Lymphoid hyperplasia infiltrados inflammatorios  affecta a toda la pared pero solo a la superficie de la mucosa y submucosa Ulcerative Colitis Histology ◦ Grossly, ulcerative colitis always involves the rectum and ◦ Histologic features of mucosal disease in ulcerative colitis extends proximally in a continuous fashion to involve part are similar to colonic Crohn disease and include or all of the colon. inflammatory infiltrates, crypt abscesses crypt distortion, and pseudopyloric epithelial metaplasia. ◦ Grossly, involved colonic mucosa may be slightly red and granular or have extensive, broad-based ulcers. ◦ The inflammatory process is diffuse and generally limited to the mucosa and superficial submucosa ◦ There can be an abrupt transition between diseased and uninvolved colon ◦ Granulomas are not present in ulcerative colitis. ◦ Isolated islands of regenerating mucosa often bulge into the lumen to create pseudopolyps ◦ Unlike Crohn disease, mural thickening is not present, the serosal surface is normal, and strictures do not occur. ◦ Inflammatory mediators can damage the muscularis propria and disturb neuromuscular function leading to colonic dilation and toxic megacolon, which carries a significant risk of perforation. Microscopic Colitis Collagenous colitis Lymphocytic colitis ◦ Occurs primarily in middle-aged and older women ◦ Lymphocytic colitis is histologically similar, but the subepithelial collagen layer is of normal thickness and the ◦ Is characterized by the presence of a dense subepithelial increase in intraepithelial lymphocytes is greater, frequently collagen layer, increased numbers of intraepithelial exceeding one T lymphocyte per five colonocytes. lymphocytes, and a mixed inflammatory infiltrate within the lamina propria ◦ Lymphocytic colitis shows a strong association with celiac disease and autoimmune diseases, including Graves disease, rheumatoid arthritis, and autoimmune or lymphocytic gastritis. These idiopathic diseases both present with chronic, nonbloody, watery diarrhea without weight loss. Radiologic and endoscopic studies are typically normal  diverticulo = pequena hernia Sigmoid Diverticular Disease de la pared digestivo - mayores diverticulosis ; diverticulitis = inflammada ▪ Acquired pseudo-diverticular outpouchings of the colonic mucosa and submucosa. ▪ Unlike true diverticula, such as Meckel diverticulum, they are not invested by all three layers of the colonic wall. ▪ Colonic diverticula are rare in persons younger than age 30, but the prevalence approaches 50% in Western adult populations older than age 60. ▪ Diverticula are generally multiple and the condition is referred to as diverticulosis. ▪ Colonic diverticula result from the unique structure of the colonic muscularis propria and elevated intraluminal pressure in the sigmoid colon. 50% a partir de los 60 anos Morphology: diverticulis ▪ Anatomically, colonic diverticula are small, flask-like outpouchings, usually 0.5 to 1 cm in diameter, that occur in a regular distribution alongside the taeniae coli. ▪ These are most common in the sigmoid colon. ▪ Colonic diverticula have a thin wall composed of a flattened or atrophic mucosa, compressed submucosa, and attenuated or, most often, totally absent muscularis propria. ▪ Hypertrophy of the circular layer of the muscularis propria in the affected bowel segment is common. ▪ Obstruction of diverticula leads to inflammatory changes, producing diverticulitis and peri-diverticulitis. ▪ Because the wall of the diverticulum is supported only by the muscularis mucosae and a thin layer of subserosal adipose tissue, inflammation and increased pressure within an obstructed diverticulum can lead to perforation.