pediagenosis: Digestive
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Showing posts with label Digestive. Show all posts
Showing posts with label Digestive. Show all posts

Friday, October 1, 2021

Celiac Disease

Celiac Disease

Celiac Disease

Celiac disease, also known as gluten-sensitive enteropathy or nontropical sprue, is a chronic immune-mediated enteropathy triggered by exposure to dietary gluten. The primary target of the disease is the small intestine; celiac disease can affect multiple systems, however.

CELIAC DISEASE AND MALABSORPTION
CELIAC DISEASE AND MALABSORPTION


It is primarily seen in individuals of European descent but is increasingly recognized on almost every continent. The overall prevalence in the general population of the United States and Europe is nearly 1%; only 10% to 15% of patients have been diagnosed and treated, however. The prevalence appears to increase with age. Celiac disease develops in genetically predisposed individuals as a result of the influence of environmental factors. First-degree relatives of patients with celiac disease have a 10% to 15% risk of developing the disease. The HLA class II genes HLA-DQ2 and HLA-DQ8, which are normally expressed on the surface of antigen cells in the gut, are the most important genetic susceptibility factors in celiac disease. HLA-DQ2 is found in 90% to 95% of patients with celiac disease, with HLA-DQ8 found in most of the remaining patients. These molecules are necessary variables predisposing a patient to the disease, which means that celiac disease is unlikely if neither molecule is present. The molecules are not, however, sufficient to cause celiac disease; they occur in 30% to 40% of the general population. Gluten is a storage protein of wheat. The alcohol-soluble fraction of gluten, gliadin, is toxic in celiac disease, along with similar proteins in barley (hordeins) and rye (secalins). These proteins are rich in glutamine and proline residues that even the healthy human intestine cannot fully digest. As a result, intact gliadin peptides are left in the lumen, but few cross the intestinal barrier. In individuals with celiac disease, these fragments come into contact with tissue transglutaminase, a ubiquitous intracellular enzyme that is released by inflammatory and endothelial cells and fibroblasts in response to mechanical irritation or inflammation. Upon contact, tissue transglutaminase cross-links with these glutamine-rich proteins and deamidates them. This process modifies glutamine residues into glutamic acid residues, which are ideally suited to interact with the HLA-DQ2 or HLA-DQ8 molecules. Once bound to HLA-DQ2 or HLA-DQ8, gliadin peptides are presented to the CD4+ T cells, triggering the inflammatory reaction. The end result is an inflammatory state of the small intestine, causing a derangement in the architecture of the mucosa, with flattening of the villi, and infiltration of lymphocytes into the epithelium.

Diverticula of Small Intestine

Diverticula of Small Intestine

Diverticula of Small Intestine

A diverticulum is a blind outpouching of a hollow viscus, consisting of one or more layers of the part involved. Small intestinal diverticula usually occur in the duodenum and occur less frequently in the jejunum and ileum. The true incidence is not known, because diverticula may remain asymptomatic and the diagnosis is usually incidental; duodenal diverticula have been reported in 7% of those undergoing endoscopic retrograde cholangiopancreatography. In about 20% of cases, they are associated with diverticula in other parts of the digestive tract.

Diverticula of Small Intestine


Diverticula of the small intestine may be single or multiple. Jejunal diverticula are usually multiple and are frequently associated with disorders of intestinal motility, such as progressive systemic sclerosis, visceral neuropathies, and myopathies. The multiple diverticula can be so numerous as to involve nearly the entire small intestine. They are located almost always along the line of mesenteric attachment, with sizes varying from a few millimeters up to several centimeters in diameter. The “complete” diverticula, formed by all the layers of the intestinal wall, are believed to be of congenital origin and are frequently associated with other malformations. The “incomplete” diverticula, consisting only of mucosa and serosa, are caused by herniation through a defect caused by the entrance of large vessels.

Meckel Diverticulum

Meckel Diverticulum

Meckel Diverticulum

The vitelline, or omphalomesenteric, duct connects the yolk sac with the primitive tubular gut in the early embryonic stages and normally involutes at about the 7th week of fetal life, leaving no trace of its existence. Failure of the vitelline duct to disappear in its entire extension results in a variety of remnants, which include a diverticulum (Meckel diverticulum) attached to the ileum, omphalomesenteric cysts (enterocysts), omphalomesenteric fistulae that drain through the umbilicus, and fibrous bands from the diverticulum to the umbilicus that predispose to bowel obstruction. The most common form is Meckel diverticulum.

VARIANTS OF VITELLINE DUCT REMNANTS
VARIANTS OF VITELLINE DUCT REMNANTS


Meckel diverticulum is the most frequent congenital anomaly of the gastrointestinal tract and is classically described by the rule of twos. It is prevalent in approximately 2% of the population, is usually located within 2 feet of the ileocecal valve, and measures approximately 2 inches in length. It is two times as prevalent in males as in females, with approximately 2% of patients developing a complication, usually within the first 2 years of life. This diverticulum is always attached to the antimesenteric side of the ileal wall, and it varies in length (from 1 to 10 cm) and also in width (from 1 to 4 cm in diameter), though its shape usually resembles that of a finger of a glove. The artery supplying the diverticulum, the vitelline artery, is a branch of the superior mesenteric artery. It crosses over the ileal wall along the diverticulum to its tip.

Duplications of Alimentary Tract

Duplications of Alimentary Tract

Duplications of Alimentary Tract

Alimentary tract duplications, also referred to as mesenteric cysts, giant diverticula, or enteric cysts, are rare congenital malformations that develop during fetal life. These spherical or tubular structures may be single or, more frequently, multiple, and are equipped with all the layers of that part of the alimentary tract to which they are intimately attached, including the muscular coat. This is in distinction to diverticula, which lack a muscular coat. Gastrointestinal duplication cysts may or may not communicate with the adjacent lumen of the gastrointestinal tract.

Duplications of Alimentary Tract


Most intestinal duplications are diagnosed in newborn infants and children, but some can remain silent and present in adulthood. With the routine use of prenatal ultrasound, however, many are being diagnosed in utero. Associated anomalies are present in one third of cases and involve the spine and gastrointestinal tract.

Omphalocele

Omphalocele

Omphalocele

Omphalocele


An omphalocele, or exomphalos, is a midline abdominal wall defect covered by a membrane of amnion and peritoneum containing bowel, and, occasionally, spleen and liver at the base of the umbilical cord. When the defect is less than 4 cm, it is termed a hernia of the umbilical cord; when it is greater than 10 cm, it is termed a giant omphalocele. It results from the persistence of the physiologic midgut herniation beyond the 12th postmenstrual week. Associated abnormalities occur in 30% to 70% of infants and include chromosomal abnormalities (trisomy 13, 18, 21), congenital heart disease, Beckwith- Wiedemann syndrome, and prune belly syndrome. The diagnosis of an omphalocele can usually be made by inspection, but if the omphalocele is small, it may appear to be a normal part of the umbilical cord. The major differential diagnosis to consider is gastroschisis. Gastroschisis is a defect in the abdominal wall that usually occurs to the right of the normal insertion area of the umbilical cord; it is believed to arise at the site of involution of the right umbilical vein. The absence of a membranous sac with free-floating loops of bowel distinguishes gastroschisis from omphalocele; if the membranous sac of the omphalocele ruptures in utero, however, other clues should be sought, such as the location of the liver and site of the cord insertion. When omphalocele is identified prenatally, fetal genetic studies, including amniocentesis and fetal echocardiography, should be offered because of the high risk of aneuploidy and other congenital and genetic disorders. Fetal growth should subsequently be monitored closely. Precluding other obstetric indications, spontaneous labor and delivery should be allowed to occur.

Intussusception

Intussusception

Intussusception

Intussusception


Intussusception occurs when a proximal segment of the bowel telescopes into an adjacent distal segment. It is one of the most common abdominal emergencies in children but is rare in adults. Intussusception commonly occurs near the ileocecal junction, where the intussusceptum telescopes into the intussuscipiens, dragging the associated mesentery with it. This leads to the development of venous and lymphatic congestion with resulting intestinal edema, which can ultimately lead to ischemia, perforation, and peritonitis. Rarely, the proximal bowel is drawn into the lumen of the distal bowel (retrograde intussusception); this phenomenon is seen in Roux-en-Y gastric bypass surgery. The majority of cases in children are idiopathic, although evidence points to a preceding viral infection triggering the intussusception in some of these cases. On the other hand, adults usually have a distinct underlying pathologic lead point, which can be malignant in half of cases. Intermittent abdominal pain is the most common presentation in both children and adults. Symptoms progress over time and are accompanied by nausea and vomiting. In children, a sausage- shaped abdominal mass may be felt in the right side of the abdomen accompanied by the “currant jelly” stool mixed with blood and mucous.

Congenital Intestinal Obstruction: Meconium Ileus

Congenital Intestinal Obstruction: Meconium Ileus

Congenital Intestinal Obstruction: Meconium Ileus

Congenital Intestinal Obstruction: Meconium Ileus


The condition known as meconium ileus develops exclusively in infants born with cystic fibrosis, which is a lethal autosomal recessive disorder caused by mutation of the cystic fibrosis transmembrane conductance regulator (CFTR) protein. This mutation primarily interferes with chloride transport in various acinar structures of the intestinal, bronchial, salivary, and sweat glands, as well as those of the pancreas. Pancreatic damage can occur in utero; 85% to 90% of these patients develop severe pancreatic insufficiency. Subsequently, the meconium becomes thick and tenacious, adhering to the intestinal mucosa and causing impaction in the ileum and intestinal obstruction.

Congenital Intestinal Obstruction: Intestinal Atresia, Malrotation of Colon, Volvulus of Midgut

Congenital Intestinal Obstruction: Intestinal Atresia, Malrotation of Colon, Volvulus of Midgut

Congenital Intestinal Obstruction: Intestinal Atresia, Malrotation of Colon, Volvulus of Midgut

Intestinal obstruction in newborn infants is caused by a variety of congenital anomalies, and prompt diagnosis and treatment can be life-saving. The causes of such intestinal obstructions may be atresia of the esophagus, diaphragmatic hernia, annular pancreas, malrotation of the colon with volvulus of the midgut, peritoneal bands mostly compressing the duodenum, internal or mesentericoparietal herniations, meconium ileus, aganglionic megacolon, imperforate anus, and atresia or congenital stenosis of the bowel.

CONGENITAL INTESTINAL ATRESIA
CONGENITAL INTESTINAL ATRESIA


Atresia refers to the complete congenital obstruction of the lumen of a hollow viscus, and stenosis refers to luminal narrowing of varying degrees. The most common site of intestinal atresia is the small bowel, particularly the jejunum and ileum; the colon is least commonly affected. Intestinal atresia results from an interruption in the normal development of the gastrointestinal tract, commonly during the second and third months of fetal life. In the proximal small bowel, this is often caused by failure of the intestine to recanalize. As the intestine changes from a solid structure to a hollow tube, one or more septa may persist, leaving a diaphragm of tissue with only a minute opening and setting up a stenosis. If such persisting septa leave an intact diaphragm across the lumen, or if, during the solid stage, the intestine divides to form two or more blind segments entirely separate from each other or connected by threadlike fibrous bands, atresia ensues. In the middle and distal small bowel, atresia often results from vascular disruption, leading to ischemic necrosis of the fetal intestine. Because the fetal bowel is sterile, the necrotic tissue is resorbed, leaving blind proximal and distal ends, often with a gap in the mesentery.

Tests for Small Bowel Function

Tests for Small Bowel Function

Tests for Small Bowel Function

TESTS OF INTESTINAL MOTILITY

Small bowel manometry, also known antroduodenal manometry, is a procedure that assesses small bowel motility. It involves placing a long tube with pressure sensors into the small intestine past the stomach. These sensors are able to measure intraluminal pressure induced by smooth muscle contractions. The test generally takes 6 hours, with the patient fasting during the first 4 hours; the patient then eats a standard meal, and a postprandial recording is made during the next 2 hours.

Tests for Small Bowel Function


The wireless motility capsule system or SmartPill Motility Monitoring system is a useful diagnostic tool that can be used to assess gut transit time. The system consists of a wireless ingestible motility capsule that the patient swallows, a portable data receiver worn by the patient for acquiring data, and data analysis software. It senses pH, temperature, and pressure, and the data can be reviewed in real time or after study completion. The small bowel transit time is defined as the time interval between capsule entry into the small bowel and its entry into the cecum. Delayed small intestinal transit is determined when transit times exceed 6 hours (range, 2 to 6 hours), based on 95% cutoff values from control studies. Small bowel scintigraphy provides valuable physiologic and quantitative information and allows the assessment of the orocecal transit time. The test involves ingestion of either a liquid or solid material labeled with 111indium or 99mtechnetium and obtaining of sequential scans over several hours. The small bowel transit time can be calculated as the time for 10% or 50% of the activity to arrive at the terminal ileum or cecum after correcting for gastric emptying. A more specific measure of duodenocecal transit involves the use of a 99mtechnetium- hepatobiliary iminodiacetic acid intravenous tracer, which is taken up by the liver and excreted in the bile directly into the duodenum; this avoids the influence of gastric emptying on scintigraphic measurement of small bowel transit; there is limited published information regarding this technique, however.

Pathophysiology of Small Intestine

Pathophysiology of Small Intestine

Pathophysiology of Small Intestine

The most important functions of the small intestine are digestion and absorption of nutrients. They are achieved by an interaction between intact small bowel motility and gastrointestinal hormones. Clinically recognizable disturbances of small bowel function arise mainly from alterations in the motor activities or interference with digestion and absorption.

 

Pathophysiology of Small Intestine

ABDOMINAL PAIN

Abdominal pain is a common manifestation of several processes involving the small intestine. The pain is often located in the mid abdomen (periumbilical region) but can also be diffuse across the abdomen. Progressive small bowel distention with or without obstruction causes colicky pain in the early stages, which later becomes constant and unrelenting. Invasive bacteria such as Yersinia can invade the terminal ileum, causing severe pain and tenderness mimicking acute appendicitis. Severe postprandial pain that incites fear of eating (sitophobia) is diagnostic of mesenteric ischemia, especially when it is accompanied by weight loss in an atherosclerotic patient. Crohn disease frequently involves the distal small bowel, with deep transmural ulceration and crampy abdominal pain in the right lower quadrant.

Gastrointestinal Hormones

Gastrointestinal Hormones

Gastrointestinal Hormones

The epithelium of the gastrointestinal tract contains multiple cell types, including specialized cells termed enteroendocrine cells that number less than 1% of the cell population and yet form the largest endocrine system of the body. Enteroendocrine cells synthesize, store, and release chemical transmitters that are involved in gastrointestinal motility, secretion, and absorption and in regulation of appetite. These transmitters are predominantly small polypeptides that are also found in the enteric nervous system and the central nervous system. There are more than 30 gut peptide hormone genes identified, which express more than 100 bioactive peptides. They are grouped into “families” according to their primary structure. In this section, the pancreatic polypeptide family will be discussed.

Gastrointestinal Hormones


Peptide YY is one of the gut peptides that belongs to the pancreatic polypeptide family of peptides, which also includes pancreatic polypeptide and neuropeptide Y. Despite sharing structural similarities and the same 36 amino acid lengths, the gut peptides vary in their biologic functions and locations. Peptide YY, neuropeptide Y, and pancreatic polypeptide bind to a family of G-protein–linked receptors (called Y receptors). At present, five receptor subtypes have been identified.

Tuesday, September 21, 2021

Motility of Small Intestine

Motility of Small Intestine

Motility of Small Intestine

MOTILITY AND DYSMOTILITY OF SMALL INTESTINE
MOTILITY AND DYSMOTILITY OF SMALL INTESTINE


The digestive status (fed versus fasting) is a key component of small bowel motility. Fasting small intestinal motility follows four cyclic phases, referred to as the migratory motor complex. The migratory motor complex consists of waves of electrical activity that sweep through the intestine every 90 to 120 minutes. In addition to facilitating the transport of indigestible substances from the stomach to the colon, the migratory motor complex also transports bacteria from the small intestine to the large intestine and inhibits the reflux of colonic bacteria to the terminal ileum. It has thereby been termed the “intestinal housekeeper.”

Lymph Drainage of Small Intestine

Lymph Drainage of Small Intestine

Lymph Drainage of Small Intestine

Lymph Drainage of Small Intestine


The lymph vessels of the small intestine begin with the central lacteals of the villi. At the base of the villi, each central lacteal joins with lymph capillaries, draining the nearby intestinal crypts. These lymph capillaries form a fine network within the lamina propria, in which the first lymphatic valves are already encountered. Many minute branches emerge from this network, penetrating through the muscularis mucosae into the submucosa, which hosts a sizable network of lymphatic vessels. The vessels of this network have conspicuous valves that prevent retrograde motion of the lymphatic fluid once it is inside the vessels. Progressively larger lymph vessels, receiving additional lymph from the layers of the muscularis mucosae and from the serosa and subserosa, pass toward the attachment of the mesentery to the small intestine. Within the mesentery, the lymph vessels travel alongside arteries and veins. These larger lymph vessels have been referred to as chyliferous vessels or lacteals because they transport emulsified fat absorbed from the intestines and appear as milky-white threads after the ingestion of fat-containing food. Lymph fluid traveling through these vessels encounters several juxtaintestinal (within the mesentery, alongside the intestines) superior mesenteric lymph nodes, which number some 100 to 200 and constitute the largest aggregate of lymph nodes in the body. They increase in number and size toward the root of the mesentery. In the root of the mesentery, larger lymphatic branches are situated, which lead into the central group of superior mesenteric nodes in the area where the superior mesenteric artery arises from the aorta.

Blood Supply of Small Intestine

Blood Supply of Small Intestine

Blood Supply of Small Intestine

Blood Supply of Small Intestine


For the typical pattern of arterial branching of the small intestines, please refer to Plates 1-1 and 1-2. In this section, we will describe the variations concerning the origin, course, anastomoses, and distribution of the vessels supplying the small intestine. These variations are so frequent that conventional textbook descriptions are inadequate for anyone attempting procedures in the area. Typically, the superior mesenteric artery supplies almost all of the small intestine aside from the proximal duodenum, which receives blood from the supraduodenal and superior pancreaticoduodenal arteries. These arteries are branches of the gastroduodenal artery, a branch of the common hepatic artery, which is itself a branch of the celiac trunk.

Structure of Small Intestine

Structure of Small Intestine

Structure of Small Intestine

MUCOSA AND MUSCULATURE OF DUODENUM
MUCOSA AND MUSCULATURE OF DUODENUM


The freely mobile portion of the small intestine, which is attached to the mesentery, extends from the duodenojejunal flexure to the ileocolic orifice, where the small intestine joins the large intestine. This portion of the small intestine consists of the jejunum and the ileum. They run imperceptibly into each other, the transition being marked by a gradual change in the diameter of the lumen and by several structural alterations.

Topography and Relations of Small Bowel

Topography and Relations of Small Bowel

Topography and Relations of Small Bowel

Topography and Relations of Small Bowel


The small intestine consists of a retroperitoneal portion, the duodenum, and a mesenteric portion made up of the coils of the jejunum and ileum. The total length of the mesenteric portion of the small intestine varies considerably. The average for adults is roughly 5 m. The proximal jejunum forms approximately two fifths of the mesenteric portion, and the ileum forms the remaining three fifths. The jejunum commences at the duodenojejunal flexure on the left side of the second lumbar vertebra or, occasionally, somewhat more cranially. The ileum terminates when it joins the large intestine in the right iliac fossa. Although the division between the jejunum and ileum is not grossly visible (the appearance of the arteries and histologic structure can be used to distinguish the two regions), the coils of the jejunum tend to be on the superior left side of the abdomen and those of the ileum on the inferior right side.

Development of Small Intestine

Development of Small Intestine

Development of Small Intestine

Development of Small Intestine


The small intestine includes the duodenum, jejunum, and ileum. During development of the gastrointestinal system, the duodenum comes from the distal portion of the foregut, whereas the jejunum and ileum come entirely from the midgut. The duodenum moves to the right of the midline as the stomach rotates and shifts to the left side of the abdomen during weeks 4 to 6 of fetal life. As development proceeds, the common bile duct moves to the posterior side of the gut tube as the stomach rotates and the liver enlarges. One aspect of duodenal development that is clinically important is that during weeks 5 and 6, the epithelial lining of the duodenum, derived from the endoderm, proliferates to the point that it completely blocks the lumen of the duodenum. However, the lumen of the duodenum typically recanalizes so that the fetus can begin swallowing amniotic fluid. If the lumen of the duodenum does not recanalize or opens incompletely, duodenal atresia or stenosis will occur. As a region of gut that links the foregut and midgut, the duodenum is supplied by branches of both the celiac and superior mesenteric arteries. The descending and horizontal portions of the duodenum are the regions where this anastomosis occurs, and these are also the regions in which atresia or stenosis is most likely to be manifested.

Physiology of Gastroenteric Stomas

Physiology of Gastroenteric Stomas

Physiology of Gastroenteric Stomas

Physiology of Gastroenteric Stomas


Creation of a well-constructed ostomy by a highly skilled surgeon at the site of an anastomosis or as a cutaneous stoma that preserves normal digestive functions can result in an excellent quality of life for a patient undergoing resection of portions of the digestive system. Technical risks associated with the creation of any stoma include anastomotic leak, dehiscence, and stricture. The size of the anastomosis varies with the organs involved and the desired outcome of the procedure, but it is important to note that while stricture-related closure is always a risk, larger stomas are not always better. Cutaneous ostomies have an additional risk of prolapse, bleeding, and peristomal ulceration. Evaluation of ostomy function and anatomy may require skilled radiologic assessment with barium studies, CT studies, or endoscopy, or a combination of these studies. Endoscopic evaluation also provides the potential for therapeutic interventions to correct stomal problems, including dilatation and placement of self-expanding stents.

Abdominal Wounds: Blast Injuries

Abdominal Wounds: Blast Injuries

Abdominal Wounds: Blast Injuries

Abdominal Wounds: Blast Injuries


Abdominal wounds and blunt trauma are common acute injuries encountered in emergency settings. The depth and severity of a penetrating wound cannot be determined by history or physical examination alone. After stabilizing the airway, breathing and circulation, emergency cross-sectional imaging is essential as the operating room is being prepared and surgical expertise recruited. Broad-spectrum intravenous antibiotics should be hung on admission as the patient is prepped for operation. If extensive intraabdominal bleeding is occurring, laparotomy should be done as early as possible. Exploration must be thorough, and all perforations must be closed. Diversion of the fecal stream is often advised when there has been peritoneal soiling. In extensive damage, resection is necessary. In addition to customary preoperative and postoperative measures, oxygen, continuous gastroduodenal suction, multiple drains, and broad-spectrum antibiotic therapy are essential.

Cancer of Peritoneum

Cancer of Peritoneum

Cancer of Peritoneum

Cancer of Peritoneum


Primary malignant tumors of the peritoneum (meso-theliomas or endotheliomas) are rare, but secondary malignant tumors are relatively common. Tumor cell spread into the peritoneum occurs by direct extension, hematogenous spread, or lymphatic spread. Once the peritoneum has been invaded, dissemination of malignant cells throughout the peritoneal cavity and implantation diffusely throughout the peritoneal surfaces can occur rapidly. Epithelial primary carcinomas commonly metastasize to the peritoneum (e.g., adenocarcinomas of the stomach, intestine, ovaries, and, less commonly, lung and breast). Melanomas also frequently metastasize to the digestive system, including the mesentery. Malignant neoplasms of the retroperitoneal connective, nervous, or muscular tissue, as well as sarcomas and teratomas, although rare, invade the peritoneum or become metastasized within it.

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