Normal Ileum
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Anatomy of Small Intestine Doctors Notes Notes/Extra Explanation Please View Our Editing File Before Studying This Lecture to Check for Any Changes
Color Code Important Anatomy of Small Intestine Doctors Notes Notes/Extra explanation Please view our Editing File before studying this lecture to check for any changes. Objectives: At the end of the lecture, students should: List the different parts of small intestine. Describe the anatomy of duodenum, jejunum & ileum regarding: the shape, length, site of beginning & termination, peritoneal covering, arterial supply & lymphatic drainage. Differentiate between each part of duodenum regarding the length, level & relations. Differentiate between the jejunum & ileum regarding the characteristic anatomical features of each of them. Abdomen What is Mesentery? It is a double layer attach the intestine to abdominal wall. If it has mesentery it is freely moveable. L= liver, S=Spleen, SI=Small Intestine, AC=Ascending Colon, TC=Transverse Colon Abdomen The small intestines consist of two parts: 1- fixed part (no mesentery) (retroperitoneal) : duodenum 2- free (movable) part (with mesentery) :jejunum & ileum Only on the boys’ slides RELATION BETWEEN EMBRYOLOGICAL ORIGIN & ARTERIAL SUPPLY مهم :Extra Arterial supply depends on the embryological origin : Foregut Coeliac trunk Midgut superior mesenteric Hindgut Inferior mesenteric Duodenum: • Origin: foregut & midgut • Arterial supply: 1. Coeliac trunk (artery of foregut) 2. Superior mesenteric: (artery of midgut) The duodenum has 2 arterial supply because of the double origin The junction of foregut and midgut is at the second part of the duodenum Jejunum & ileum: • Origin: midgut • Arterial -
Short Bowel Syndrome with Intestinal Failure Were Randomized to Teduglutide (0.05 Mg/Kg/Day) Or Placebo for 24 Weeks
Short Bowel (Gut) Syndrome LaTasha Henry February 25th, 2016 Learning Objectives • Define SBS • Normal function of small bowel • Clinical Manifestation and Diagnosis • Management • Updates Basic Definition • A malabsorption disorder caused by the surgical removal of the small intestine, or rarely it is due to the complete dysfunction of a large segment of bowel. • Most cases are acquired, although some children are born with a congenital short bowel. Intestinal Failure • SBS is the most common cause of intestinal failure, the state in which an individual’s GI function is inadequate to maintain his/her nutrient and hydration status w/o intravenous or enteral supplementation. • In addition to SBS, diseases or congenital defects that cause severe malabsorption, bowel obstruction, and dysmotility (eg, pseudo- obstruction) are causes of intestinal failure. Causes of SBS • surgical resection for Crohn’s disease • Malignancy • Radiation • vascular insufficiency • necrotizing enterocolitis (pediatric) • congenital intestinal anomalies such as atresias or gastroschisis (pediatric) Length as a Determinant of Intestinal Function • The length of the small intestine is an important determinant of intestinal function • Infant normal length is approximately 125 cm at the start of the third trimester of gestation and 250 cm at term • <75 cm are at risk for SBS • Adult normal length is approximately 400 cm • Adults with residual small intestine of less than 180 cm are at risk for developing SBS; those with less than 60 cm of small intestine (but with a -
Anatomy of the Small Intestine
Anatomy of the small intestine Make sure you check this Correction File before going through the content Small intestine Fixed Free (Retro peritoneal part) (Movable part) (No mesentery) (With mesentery) Duodenum Jejunum & ileum Duodenum Shape C-shaped loop Duodenal parts Length 10 inches Length Level Beginning At pyloro-duodenal Part junction FIRST PART 2 INCHES L1 (Superior) (Transpyloric Termination At duodeno-jejunal flexure Plane) SECOND PART 3 INCHES DESCENDS Peritoneal Retroperitoneal (Descending FROM L1 TO covering L3 Divisions 4 parts THIRD PART 4 INCHES L3 (SUBCOTAL (Horizontal) PLANE) Embryologic Foregut & midgut al origin FOURTH PART 1 INCHES ASCENDS Lymphatic Celiac & superior (Ascending) FROM L3 TO drainage mesenteric L2 Arterial Celiac & superior supply mesenteric Venous Superior mesenteric& Drainage Portal veins Duodenal relations part Anterior Posterior Medial Lateral First part Liver Bile duct - - Gastroduodenal artery Portal vein Second Part Liver Transverse Right kidney Pancreas Right colic flexure Colon Small intestine Third Part Small intestine Right psoas major - - Superior Inferior vena cava mesenteric vessels Abdominal aorta Inferior mesenteric vessels Fourth Part Small intestine Left psoas major - - Openings in second part of the duodenum Opening of accessory Common opening of bile duct pancreatic duct (one inch & main pancreatic duct: higher): on summit of major duodenal on summit of minor duodenal papilla. papilla. Jejunum & ileum Shape Coiled tube Length 6 meters (20 feet) Beginning At duodeno-jejunal flexur -
Acute Terminal Ileitis Mimicking Crohn's Disease Caused By
Case Report Acute Terminal Ileitis Mimicking Crohn’s Disease Caused by Salmonella veneziana Daniele Dionisio, MD; * Francesco Esperti, MD; * Angela Vivarelli, MD; * Claudio Fabbri, MD; * Paola Apicella, MD;I Nicola Meola, MD, *** Patrizia Lencioni, PhD,§ and Roberto Vannucci, MDn Gastroenteritis induced by nontyphoidal Salmonella is mesenterium and adjoining small bowel (Figure 1). Stool characterized by fluid secretion and inflammatory neu- cultures established the diagnosis of Salmonella species trophil migration into the intestinal mucosa and the gut enterica subspecies enter&a serotype veneziana (11: i: lumen. l-3 Nontyphoidal Salmonella may specifically enx),‘” with negative results for mycobacteria, Clostrid- infect the terminal ileum (terminal ileitis) or the ileocecal ium di@cile toxins, fungi, parasites, adenoviruses, and area (ileocecitis), thus mimicking appendicitis and rotaviruses. For Salmonella, after incubation in selenite Crohn’s disease.*-’ Superinfection with these agents in broth (Selenite Broth, Biolife, Milan, Italy), the stool sam- relapses of inflammatory bowel disease has been ples were passed in solid SM ID medium (Salmonella reported.X In addition, Salmonella may cause appendici- Identification Agar, Biomerieux-Marcy D’Etoile, Paris, tis by direct invasion of the appendix.9 No reports of animal or human infections caused by Salmonella veneziana are currently available, although some cases of human infection have been diagnosed by stool cultures in Italy To the authors’ knowledge, no gut biopsies were taken in these cases, and nothing was known about environmental sources, clinical manifesta- tions, host predisposing factors, drug susceptibility pat- terns, or duration of microbial shedding in feces. Because of the lack of information, the natural history of infection caused by S. -
What Is an Enteral Feeding Tube?
Your Feeding Tubes Feeding Your What Is an Enteral Feeding Tube? Enteral refers to within the digestive system or intestine. Enteral feeding tubes allow liquid food to enter your stomach or intestine through a tube. The soft, flexible tube enters a surgically created opening in the abdominal wall called an ostomy. An enterostomy tube in the stomach is called a gastrostomy. A tube in the small intestine is called a jejunostomy. The site on the abdomen where the tube is inserted is called a stoma. The location of the stoma depends on your specific operation and the shape of your abdomen. Most stomas: f Lie flat against your body f Are round in shape f Are red and moist (similar to the inside of your mouth) f Have no feeling Gastrostomy feeding tube Stoma tract Surgical Patient Education 112830_BODY.indd 1 8/21/15 9:25 AM 3 Who Needs an Enteral Feeding Tube? Cancer, trauma, nervous system and digestive system disorders, and congenital birth defects can cause difficulty in feeding. Some people also have difficulty swallowing, which increases the chance that they will breathe in food (aspirate). People who have difficulties feeding can benefit from a feeding tube. Your doctor will explain to you the specific reasons why you or your family member need a feeding tube. For some, a feeding tube is a new way of life, but for others, the tube is temporary and used until the problem can be treated or repaired. Low-profile feeding tube American College of Surgeons • Division of Education 112830_BODY.indd 2 8/21/15 9:25 AM 2 Your Feeding Tubes Feeding Your Understanding Your Digestive System When food enters your oral cavity (mouth), the lips and tongue move it toward the back of the throat. -
Psoas Fistula and Abscess in a Patient with Crohn's Disease Presenting As
314 ANNALS OF GASTROENTEROLOGYD. CHRISTODOULOU 2001, 14(4):314-318 et al Case report Psoas fistula and abscess in a patient with Crohns Disease presenting as claudication and hip arthritis D. Christodoulou1, N. Tzambouras1, K. Katsanos1, I. Familias1, K. Tsamboulas,2 E.V. Tsianos1 SUMMARY Abbreviations: CRP: C reactive protein, ESR: Eryth- rocyte sedimentation rate, US: Ultrasonography, CT: Crohns disease is characterized by chronic intestinal in- Computed Tomography, MRI: Magnetic Resonance flammation and not rarely by extraintestinal manifesta- Imaging. tions. Psoas abscess and fistula is a rare complication of Crohns disease, which is sometimes difficult to diagnose INTRODUCTION in the early stage. We describe the case of a 22-year-old male patient with Crohns disease who presented to us with Crohns disease is characterized by a chronic inflam- difficulty in walking and pain in the area of the right hip. A mation of the bowels, which extends to the deeper layers MRI scan of the hip joints was negative for aseptic necro- of the intestinal wall.1 It may involve every part of the sis of the head of femur. An ultrasound examination of the gastrointestinal tract, but in the majority of cases it mainly lower abdomen was also negative, as were the X-rays of the affects the terminal ileum and/or the colon. The disease sacral bone and sacroiliac joints. The patient was treated is characterized by the presence of extraintestinal mani- with non-steroidal anti-inflammatory agents but his con- festations and perianal complications in about 30% of dition worsened and he developed diarrhoea. Subsequent- patients,2 as well as the development of intra-abdominal ly, he developed fever and local tenderness of soft tissues or pelvic abscesses in 10-30%.3 The activity of intestinal of the right hip and buttock. -
Digestive System A&P DHO 7.11 Digestive System
Digestive System A&P DHO 7.11 Digestive System AKA gastrointestinal system or GI system Function=responsible for the physical & chemical breakdown of food (digestion) so it can be taken into bloodstream & be used by body cells & tissues (absorption) Structures=divided into alimentary canal & accessory organs Alimentary Canal Long muscular tube Includes: 1. Mouth 2. Pharynx 3. Esophagus 4. Stomach 5. Small intestine 6. Large intestine 1. Mouth Mouth=buccal cavity Where food enters body, is tasted, broken down physically by teeth, lubricated & partially digested by saliva, & swallowed Teeth=structures that physically break down food by chewing & grinding in a process called mastication 1. Mouth Tongue=muscular organ, contains taste buds which allow for sweet, salty, sour, bitter, and umami (meaty or savory) sensations Tongue also aids in chewing & swallowing 1. Mouth Hard palate=bony structure, forms roof of mouth, separates mouth from nasal cavities Soft palate=behind hard palate; separates mouth from nasopharynx Uvula=cone-shaped muscular structure, hangs from middle of soft palate; prevents food from entering nasopharynx during swallowing 1. Mouth Salivary glands=3 pairs (parotid, sublingual, & submandibular); produce saliva Saliva=liquid that lubricates mouth during speech & chewing, moistens food so it can be swallowed Salivary amylase=saliva enzyme (substance that speeds up a chemical reaction) starts the chemical breakdown of carbohydrates (starches) into sugar 2. Pharynx Bolus=chewed food mixed with saliva Pharynx=throat; tube that carries air & food Air goes to trachea; food goes to esophagus When bolus is swallowed, epiglottis covers larynx which stops bolus from entering respiratory tract and makes it go into esophagus 3. -
Stone Ileus: an Unusual Presentation of Crohn's Disease
Ma, et al. Int J Surg Res Pract 2016, 3:046 International Journal of Volume 3 | Issue 2 ISSN: 2378-3397 Surgery Research and Practice Case Report: Open Access Stone Ileus: An Unusual Presentation of Crohn’s Disease Charles Ma and H Tracy Davido Department of Critical Care and Acute Care Surgery, University of Minnesota Health, USA *Corresponding author: H Tracy Davido MD, Assistant Professor of Surgery, Department of Critical Care and Acute Care Surgery, University of Minnesota Health, 11-115A Phillips Wangensteen Building, 420 Delaware St. SE, MMC 195, Minneapolis, MN 55455, USA, Tel: 612-626-6441, E-mail: [email protected] Introduction Case Report Stone ileus, also known as enterolith ileus enterolithiaisis, is a rare A 67-year-old morbidly obese woman came to the emergency complication of cholelithiasis and an even rarer symptom of Crohn’s department at our institution with an upper respiratory infection, disease. Gallstone ileus is secondary to fistula formation between decreased appetite, and malaise. Her past medical history was the gallbladder and the gastrointestinal (GI) system. Enterolithiasis significant for an open cholecystectomy more than 30 years earlier. of Crohn’s disease is thought to arise from the stasis of succus She had no additional past surgical history or diagnoses. The initial within the small bowel eventually leading to stone formation and workup revealed acute renal failure, with significant electrolyte growth. Both gallstone ileus and enterolithiasis of Crohn’s disease abnormalities and dehydration. She underwent intravenous fluid can result in subsequent mechanical bowel obstruction. Gallstone resuscitation and electrolyte replacement in the Medical Intensive ileus accounts for 1% to 4% of mechanical bowel obstructions, with Care Unit; however, while hospitalized, she developed new-onset higher a incidence in women over age 60 [1]. -
Hepatic Portal Venousgasdisappearing Within
CASE REPORT Hepatic Portal Venous Gas Disappearing within 24 Hours Miyako Niki, Ichiro Shimizu*, Takahiro Horie, Michiyo Okazaki, Tatsuhiko Shiraishi, Hisashi Takeuchi, Soichiro Fujiwara, Masahiko Murata, Koji Yamamoto, Arata Iuchi, Yoshio Atagi** and Susumu Ito* Abstract the time of the admission, abdominal pain had already disap- peared. Her abdomenwas flat and soft, and neither tenderness Hepatic portal venous gas (HPVG)was detected by CT nor muscular defense was noted. The patient did not complain in a 64-year-old womanwho suddenly complained of lower of fever, and no other specific physical abnormalities were abdominal pain. However, the abdominal symptoms dis- observed. Hematological and biochemical examinations indi- appeared rapidly, and lower gastrointestinal endoscopy in- cated slight leukocytosis (WBC 9,630/|il) with neutrophilia dicated only terminal ileitis. Conservative treatment alone (neutrophil 82.9%), although CRPlevels (0. 1 mg/dl) were nor- was performed, and HPVGcompletely disappeared ap- mal. In addition, anemicfindings were not evident, and both proximately 18 hours later. The use of CTproved to be use- liver and renal functions appeared to be normal. Abdominal ful for following the course of HPVG. ultrasonography demonstrated high spot echo entry findings (Internal Medicine 41: 950-952, 2002) in the portal vein (Fig. 2). Abdominal CT performed at around 5:00 PMdemonstrated a slightly diminished dendritic gas im- Key words: hepatic portal venous gas, 24 hours, ileitis age in the liver, which was observed on CTat a local clinic (Fig. IB). Based on these subjective and objective findings, the patient was diagnosed as having HPVGwithout any ac- companyingsevere pathologic conditions such as intestinal Introduction necrosis that would require emergencysurgery. -
GI Tract Anatomy
SHRI Video Training Series 2018 dx and forward Recorded 1/2020 Colorectal Introduction & Anatomy Presented by Lori Somers, RN 1 Iowa Cancer Registry 2020 Mouth GI Tract Pharynx Anatomy Esophagus Diaphragm Liver Stomach Gallbladder Pancreas Large Small Intestine Intestine (COLON) 2 Anal Canal 1 Colorectal Anatomy Primary Site ICD-O Codes for Colon and Rectum Transverse Hep. Flex C18.4 Splen. Flex C18.3 C18.5 Ascending Large Descending C18.2 Intestine, C18.6 NOS C18.9 Cecum C18.0 Sigmoid C18.7 Appendix C18.1 Rectum C20.9 Rectosigmoid C19.9 3 ILEOCECAL JUNCTION ILEUM Ileocecal sphincter Opening of appendix APPENDIX 4 2 Rectum, Rectosigmoid and Anus Rectosigmoid junction Sigmoid colon Peritoneal Rectum reflection Dentate line Anus 5 Anal verge Peritoneum: serous membrane lining the interior of the abdominal cavity and covers the abdominal organs. Rectum is “extraperitoneal” Rectum lies below the peritoneal reflection and outside of peritoneal cavity 6 3 Greater Omentum Liver Stomach Vessels Ligament Greater Omentum: (reflected upward) Gallbladder Greater Greater Omentum Omentum Transverse colon coils of jejunum Ascending Descending colon colon Appendix Cecum coils of ileum slide 9 slide 10 7 Mesentery (Mesenteries): folds of peritoneum- these attach the colon to the posterior abdominal wall. Visceral peritoneum: = Serosa covering of colon (organs) Parietal peritoneum: = Serosa covering of ABD cavity (body cavities) 8 4 Colon & Rectum Wall Anatomy Lumen Mucosa Submucosa Muscularis propria Subserosa Serosa Peritoneum 9 Layers of Colon Wall -
Hepatobiliary Manifestations and Complications in Inflammatory Bowel Disease: a Review
Review Gastroenterol Res. 2018;11(2):83-94 Hepatobiliary Manifestations and Complications in Inflammatory Bowel Disease: A Review Fotios S. Fousekisa, Vasileios I. Theopistosa, Konstantinos H. Katsanosa, Epameinondas V. Tsianosa, Dimitrios K. Christodouloua, b Abstract manifestations are reported in more than one-third of patients with IBD [1]. A varied heterogenous group of hepatobiliary Liver and biliary track diseases are common extraintestinal manifesta- manifestations has been reported in both UC and CD [2] and ap- tions of inflammatory bowel disease (IBD), reported both in Crohn’s proximately 5% of adults with IBD have developed chronic liver disease and ulcerative colitis, and may occur at any time during the disease [3]. The pathogenesis of IBD-associated liver disorders natural course of the disease. Their etiology is mainly related to patho- is unclear. Immunological, genetic and environmental factors physiological changes induced by IBD, and secondary, due to drugs may contribute to the pathogenesis and correlation between used in IBD. Fatty liver is considered as the most frequent hepatobil- IBD and hepatobiliary manifestations [4]. The most associated iary manifestation in IBD, while primary sclerosing cholangitis (PSC) hepatobiliary manifestation is primary sclerosing cholangitis is the most correlated hepatobiliary disorder and is more prevalent in (PSC), particularly in UC. Other less frequent IBD-associated patients with ulcerative colitis. PSC can cause serious complications hepatobiliary disorders include cholelithiasis, -
The Liver in Pediatric Gastrointestinal Disease
INVITED REVIEW The Liver in Pediatric Gastrointestinal Disease Hanh D. Vo, Jiliu Xu, Simon S. Rabinowitz, Stanley E. Fisher, and Steven M. Schwarz ABSTRACT well-known clinicopathologic associations. This monograph high- Hepatic involvement is often encountered in gastrointestinal (GI) dis- lights important aspects of the pathogenesis, diagnosis, and present eases, in part because of the close anatomic and physiologic relations management of hepatobiliary abnormalities associated with 3 com- between the liver and GI tract. Drainage of the mesenteric blood supply to mon GI disorders in the pediatric population: IBD, celiac disease, the portal vein permits absorbed and/or translocated nutrients, toxins, and cystic fibrosis (CF). Less frequently encountered hepatobiliary bacterial elements, cytokines, and immunocytes to gain hepatic access. manifestations of infectious and autoimmune GI disorders are listed Liver problems in digestive disorders may range from nonspecific hepa- in Table 1, but are beyond the scope of this review. tocellular enzyme elevations to significant pathologic processes that may progress to end-stage liver disease. Hepatobiliary manifestations of primary GI diseases in childhood and adolescence are not uncommon HEPATIC MANIFESTATIONS OF IBD and include several well-described associations, such as sclerosing cho- IBD encompasses a group of chronic inflammatory diseases langitis with inflammatory bowel disease. Liver damage may also result of the GI tract that includes Crohn disease (CD), ulcerative colitis from the effects of drugs used to treat GI diseases, for example, the (UC), and indeterminate colitis. Hepatic and biliary tract abnorm- hepatotoxicity of immunomodulatory therapies. This review highlights alities (Table 2) may represent part of the overall disease process in the important features of the hepatic and biliary abnormalities associated these disorders, or may occur as a consequence of medical therapy.