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THE DIGESTIVE SYSTEM

Maria Victoria M. Villarica MD
OLFU College of Medicine
Department of Pediatrics

Pediatric Module on the Digestive System

• Grading system: Written examination
A. quizzes - 5 long quiz (25 items) 40%
B. shifting exam 60%
class standing: 100%
 Textbook: Nelson Textbook of Pediatrics 19th ed.
by: Kleigman, Stanton, St. Geme, Schor, Behrman

Course Outline:
• Mouth
• Esophagus
• GIT
• Anus and Rectum
• Liver
• Gallbladder
• Pancreas

Normal Digestive Phenomena
• GI function varies with maturity
• Toungue is thrust upward and outward  backwards
• 1 month old – sweet and salty
• Complimentary feeds – 6 mos.
• Burping – encouraged to prevent gastric distention

Major Symptoms and Signs of Digestive Tract Disorders .

tumor: extrinsic: compression from vascular rings. globus • Oropharyngeal dysphagia – transfer (mouth to esophagus) due to neurologic and muscular disorders aspiration • Esophageal dysphagia – neuromuscular disorders (achalasia. odynophagia.Dysphagia – difficulty in swallowing. mediastinal lesions or vertebral abnormalities) . collagen disorders) or mechanical obstruction (intrinsic: stricture. web.

pneumomediastinum/pneumothorax. theories  Differential diagnosis – GI abnormalities. age onset: 2-5yrs old. infection). propanolol. nephrolithiasis. etc  Laboratory evaluation – based on history and PE: endoscopy. medulla and direct: afferent innervations and indirect: CTZ and higher CNS centers  Cyclic vomiting: syndrome with numerous episodes of vomiting interspersed with well intervals. metabolic-endocrine disorders. esophagitis. organic acids. metabolic studies (lactate. lifestyle changes  Potential complications – metabolic. amitriptyline. phenobarbital). prophylactic meds (cyproheptadine. occurs 1 hr to 10 days and occurs 1 week apart. return to baseline. precipitants (stress. GI radiography. ammonia)  Management – hydration and antiemetics (ondansetron). not associated with another disorder.Vomiting : reflex process. aspiration. Mallory-Weiss tear. petechiae/retinal hgges . criteria (at least 2): 5 attacks in any interval or minimum of 3 in 6mos. bile-stained – 2nd part of the duodenum  Highly coordinated reflex process preceded by  salivation and involuntary retching. brain MRI. nutritional. CNS disorders. > 4x/hr at > 1hr. shock.

hypothalamus  Diarrhea – excessive loss of fluid and electrolytes in the stool. LES • Rumination . chronic or persistent lasts >14 days .to chew  Anorexia – prolonged lack of appetite. acute (>10ml/kg/day in infants and >200ml/kg/day in older children) lasts <14 days.• Regurgitation – effortless movement of stomach contents into the esophagus and mouth.

Campylobacter. motility) – Short bowel syndrome. osmotic – maldigestion. decreased surface area (osmotic. blood and WBC. thyrotoxicosis) or delayed (pseudo- obstruction. ingestion of unabsorbable substances (lactose def. normal osmolality. <100mOs/kg ion gap b. mucosal invasion – Salmonella.celiac disease e. Amoeba. etc). lower-volume diarrhea  Mechanisms of diarrhea: a. motility . lesser volume d. electrolyte transport ( cholera toxin. voluminous diarrhea  LI – absorbs 0. rotavirus. persists with fasting. transport defects. inflammation.Diarrhea  SI –absorbs 10-11L/day of water.. >100mOs/kg ion gap c. secretion. stops with fasting.5L/day of water. colonic reabsorption. acidic. secretory . Yersinia. motility disorders – rapid (IBS.Shigella. lesser volume. etc). large volume. high osmolality. blind loop).absorption.

causes (non- organic and organic)  Neonatal period: Hirschsprung disease. hypothyroidism  Defective rectal filling: ineffective colonic peristalsis colonic stasis (excessive drying lessens the sensitivity)  Defect in emptying: failure of defecation reflex (lesions in rectal muscle. frequency and difficulty in passing stool  defects on filling or emptying the rectum. sacral spinal cord or abdominal and pelvic muscles)  Involuntary encopresis  Generates ANXIETY . depends on stool consistency.Constipation  relative definition. intestinal pseudo- obstruction.

peritoneum. C fibers – viscera. melena (blackened stools- duodenum or above distal ileum)  Abdominal distention – ascites – fluid in the peritoneal cavity  jaundice . hematochezia (distal bleeding site or above distal ileum). aching. dermatome). Abdominal pain – skin and muscle – A fibers – sharp. stomach. duodenum). localized pain. poorly localized pain. visceral pain (dull. muscle – dull. somatic pain (inflammed viscus) and referred pain (extraintestinal locations)  Gastorintestinal hemorrhage – hematemesis (esophagus.

urinary tract (inguinal area. transverse colon  Somatic Pain – peritonitis: rigidity. pancreas (back). appendix. stomach. upper bowel b. umbilicus – distal small bowel. suprapubic – distal large bowel. cecum.Abdominal Pain  Acute and Chronic  Visceral Pain: radiation of pain is helpful a. same side). cutaneous hyperesthesia  Referred Pain – parietal pleura in pneumonia . epigastrium – liver. biliary tree (right scapula). pelvic organs. rebound tenderness. involuntary muscle guarding. proximal colon c.

colonoscopy. tachycardia. Mallory- Weiss lesion • Diagnostics: EGD (esophagogastroduodenoscopy). prolapse gastropathy. breakdown products: bilirubin . tagged RBC scan.Gastrointestinal Hemorrhage • Erosive damage to the mucosa – most common cause • Others: variceal bleeding. hypotension. guaiac test (blue color) • Complications: iron-deficiency anemia.

supernumerary teeth • Radiographic examination .Oral Cavity: Teeth • Dental laminae (mesenchyme)/ectoderm – 12 wk fetal life. maxillary: central incisor at 7 ½ mos. • Anomalies: anodontia.. 20 primary teeth • Eruption: primary dentition: mandibular: central incisor at 6 ½ mos. maxillary: 1st molar at 6-7 yrs. permanent dentition: mandibular: central incisor and 1st molar at 6-7 yrs.

grooves and pits. abrasion • Dentinogenesis imperfecta – hereditary. enamel defects. bluish- opalescent sheen on poorly calcified dentin .Anomalies Associated with Tooth Development • Twinning – 2 teeth are joined together  Germination – division of 1 tooth gem to form a bifid crown  Fusion – joining of incompletely developed teeth due to crowding. pressure or trauma  Concrescence – attachment of root of adjacent teeth by an excessive deposit of cementum • Macrodontia/Microdontia/Peg-shaped laterals • Amelogenesis imperfecta – hereditary.

>0. lacy patches on the enamel to severe brownish discoloration and hypoplasia. malnutrition. associated with cleft palate.05mg/kg/day fluoride or >2. premature birth or birth trauma:  Hypocalcification – opaque. white patches or horizontal line on the tooth  Hypoplasia – more severe. etc • Neonatal teeth – erupt 1st month of life. mandibular central incisors. Pierre-Robin synd. pitting or areas devoid of enamel • Fluorosis – inconspicuous white. toothpaste. red-brown (prophyria). flouride rx) • Discolored teeth – black (neonatal hyperbil).  Riga-Fede disease – tip of tongue is amputated/lacerated .0ppm (water..• Anomalies in tooth development due to illness. brown-yellow (tetracycline) • Natal teeth – at birth.

artificial nipples • Surgery: 3 mos. soft. a syndrome malformation complex or genetic factors (IRF6 gene) • Unilateral (L>R) or bilateral and can involve the alveolar ridge • FEEDING – plastic obturator. of age . resulting to failure of the medial nasal and maxillary process to join • M>F • Causes: maternal drug exposure.Cleft Lip • Hypoplasia of the mesenchymal layer. revised at 4-5 yrs. Millard rotation-advancement technique. of age.

morphology of surrounding areas. neuromuscular function of soft palate and pharyngeal walls). associated with cleft lip • FEEDING – plastic obturator. of age. prosthetics (missing teeth). artificial nipples • Surgery: Timing is individualized (width. adequacy of existing palatal segments. soft. < 1 yr.Cleft Palate • Failure of the palatal shelves to approximate or fuse • Isolated (midline). reduction of nasal regurgitation and avoidance of injury to the growing maxilla. speech therapy . intelligible and pleasant speech. GOALS: union of cleft segments.

y or s.d.sh.h.ch or cats.boats.y or s.b.t. sisters) .h.b.ch or cats.Sequelae: Cleft Lip: Misarticulation and velopharyngeal dysfunction (cleft lip and palate) (p.t. sisters) Cleft Palate: • Recurrent otitis media and subsequent hearing loss • Displacement of maxillary arches and malposition of the teeth (orthodontic correction) • Misarticulation and velopharyngeal dysfunction (cleft lip and palate) (p.sh.d.boats.

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Post-operative Management: • Gentle aspiration of the nasopharynx minimizes atelectasis or pneumonia • Maintenance of a clean suture line and avoidance of tension on the sutures • Infant is fed with a mead-Johnson bottle • Arms are restrained • Fluid or semifluid diet X 3 weeks .

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s. otitis media.Velopharyngeal Dysfunction • Speech disturbance • Hypernasal speech.t.d. p. gargle. nasoendoscopy • Surgery: pharyngoplasty (retropositioning of palate) .f. inability to whistle. blow out a candle or inflate a balloon. loss of liquid through the nose when drinking.h.b.v. hearing loss • Radiographic studies (true lateral view).

flouride (1ppm). dental sealant . mutans.Dental caries • Interrelationship between tooth surface. avoid fruit juice (<6oz/day). by-product: glucan (polymer that enables bacteria to adhere to tooth structures) • < 3yrs old: requires restraint. lactobacilli) • Reduces pH of dental plaque demineralization cavitation • Sucrose (most cariogenic sugar). dietary carbohydrates and specific oral bacteria (Strep. By pedia. daily brushing. sedation or general anesthesia • Prevention: screening < 3yrs.

Periodontal Diseases • Gingivitis • Periodontitis (inflammation of the periodontal ligament resulting in loss of alveolar bone) • Teething: excessive salivation. low-grade fever. irritability. give oral analgesics. ice rings .

Dental Trauma • Concussion . reduction and fixation • Avulsion – replant within 20mins after injury Endodontic therapy .gentle hitting of tooth with an instrument • Sublaxation – horizontal and/or vertical mobility • Intrusion – pushed up into the socket • Extrusion – displacement of tooth from socket.

lesions – inflamed and has pinpoint hemorrhages. management: benzocaine and topical lidocaine. genetics. tetracycline use (caution) .2% chlorhexidine solution and systemic antifungals • Aphthous ulcers – canker sore. emotional stress. soft tissue injury. white plaques covering all or part of the oropharyngeal mucosa. heals without scarring. lasts 10-14 days. KOH smears. management: 0. allergic or immunologic reactions. albicans.Common Lesions of the Oral Soft Tissues • Oropharyngeal Candidiasis – C. well circumscribed ulcerative lesions with a white necrotic base surrounded by a red halo. neonates.

candidiasis .

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cheilitis .

mucocutaneous margin and perioral skin with fever. scaling. contact sensitivity. interferes with speech and feeding. disappears • Parulis – gum boil • Cheilitis – dryness of the lips. short lingual frenulum. spontaneous or may require surgery • Geographic tongue and Fissured tongue . cracking. mucosal hemorrhages and clusters of small vesicles. disappears • Dental lamina cysts – epithelial remnants of dental lamina. vit def.• Herpetic gingivostomatitis –erythematous gingiva. weakened immune system. lymphadenopathy and difficulty of eating and drinking • Bohn nodules – remnants of mucosal gland tissue. fungal/bacterial infection • Ankyloglossia – tongue-tie. burning sensation.

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END OF 1ST SESSION .

Esophagus • Hollow. muscular tube that conveys ingested material from the mouth into the stomach .

50% associated with TEF • Presentation: frothing and bubbling at the mouth and nose. cyanosis and respiratory distress • Sequelae: aspiration pneumonitis • Diagnosis:inability to pass a NGT/OGT.Esophageal atresia with TEF • Esophageal atresia – most common (esophagus). maternal polyhydramnios. plain Xray: coiled feeding tube or air-distended stomach or scaphoid abdomen . episode of coughing.

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anastomotic stricture.• Management: > maintain patent airway > prevent aspiration of secretions > surgical ligation and end-to-end anastomosis of the esophagus > ET intubation is C/I > If surgery cannot be done. reactive airway disease from GERD . primary repair cannot be done • Outcome: post-op: anastomotic leak. refistulization. a primary closure can be delayed by temporizing with fistula ligation and gastrostomy tube placement > If gap is > 3-4cm.

eosinophilic esophagitis .Obstructing and Motility Disorders of the Esophagus – compress • Obstructing lesions produce dysphagia to solids earlier than liquids • Diagnosis: radiographic studies • Extrinsic causes: esophageal duplication cysts: leads to respiratory distress because of compression of airways. congenital webs/ring. vascular anomalies (dysphagia lusoria: subclavian artery or aortic arch) • Intrinsic causes: peptic stricture. cricopharyngeal achalasia. Schatzki ring (thin bands at squamocolumnar junction). mediastinal or subcarinal lymph nodes.

Dysmotility • Cricopharyngeal achalasia (UES) –failure to relax • Cricopharyngeal incoordination (chalasia) –full relaxation of UES Diagnosis: manometry. videofluoroscopic evaluation of swallowing • Cricopharyngeal spasm – Arnold-Chiari malformation. due cranial decompression. may lead to Zenker diverticulum .

Ca-channel blockers and PDE-inhibitors. endoscopic injection of Botulinum toxin .Dysmotility (LES) • Achalasia – loss of LES relaxation and loss of esophageal peristalsis  Causes: degenerative autoimmune and infections  Manifestations: regurgitation and dysphagia (solids and liquids) with respiratory symptoms. esophagitis  Chest xray: air-fluid level in dilated esophagus  Barium fluoroscopy: “bird’s beak”  Manometry –most sensitive diagnostic test. high LES pressure and low –amplitude esophageal body contractions  Treatment: Pneumatic dilatation (initial tx of choice) and surgical (Heller) myotomy.

Achalasia (“bird’s beak”) .

Hiatal Hernia • Herniation of the stomach through the esophageal hiatus. type 1 or sliding hernia:gastroesophageal junction slides into the thorax . type 3 • GERD – problem • Symptoms: fullness after eating and upper abdominal pain • Management: medical (GERD) and correction of hernia at fundoplication . type 2: paraesophageal or the stomach fundus next to the esophagus.

Hiatal hernia .

multichannel intraluminal impedance. endoscopy. Barium radiographic studies. gagging. respiratory symptoms • Diagnostics: manometry. feeding aversion. extended esophageal pH monitoring. failure to thrive). laryngotracheobroncoscopy .GERD • Most common esophageal disorders in children (all ages) • Retrograde movement of gastric contents across the LES into the esophagus. arching. physiologic vs pathologic • Antireflux barriers: LES + crura of the diaphragm at gastroesophageal junction • Manifestations: esophagitis (irritability. choking.

prokinetic (metoclopramide (tardive dyskinesia). hypoallergenic diet). PPI (most potent antireflux drug). positioning (seated is avoided. Barrett esophagus (metaplastic transformation: squamous to columnar). H2RA. nutritional.GERD • Management: dietary measures (feeding technique. prone and upright carried position • Drugs: antacids. baclofen (centrally-acting GABA agonist • Surgery : fundoplication (radiofrequency therapy – Stretta procedure) • Complications: esophagitis: stricture. supine to left side. erythromycin. respiratory presentations . is recommended). betanechol. thickened formulas + 1 tbsp rice cereal/oz . weight reduction.

stomach. large bowel until mid-transverse colon). hindgut (remainder of the colon and anal canal) . midgut (jejunum. ileum. duodenum). completed by 8th week AOG • Foregut (esophagus.Stomach • Embryology: starts at 4th week AOG.

parallel streaks of barium in narrowed channel . with blood types B and O. Zellweger syndrome. firm. -2cm mass from the left side and located above and to the right of the umbilicus in the midepigastrium beneath the live edge • Imaging studies: UTZ and contrast studies (string sign – elongated pyloric channel.Hypertrophic Pyloric Stenosis • M>F. double-tract sign. hyperbilirubinemia (icteropyloric syndrome) – most common clinical association • Diagnosis: palpation of an “olive-shaped”. etc. shoulder sign – bulge of the pyloric muscle into the antrum. associated with Apert syndrome. not present at birth. trisomy 18. movable. familial. progressive vomiting (3 week old) leading to hypochloremic metabolic alkalosis. erythromycin use • Manifestations: nonbilous vomiting (initial symptom).

hiatal hernia. duodenal stenosis • Treatment: preoperative treatment: nasoduodenal feedings. for incomplete pyloromyotomy. endoscopic balloon dilatation is done . correcting fluid. vomiting stops when the stomach is empty • Surgery: pyloromyotomy (Ramstedt procedure). adrenal insufficiency. inborn errors of metabolism. feeding can be initiated 12-24 hrs after surgery. acid-base and electrolyte. AGE.• Differential diagnosis: GERD.

surgical or endoscopic repair once stable . • nonbilious vomiting. LBW and epidermolysis bullosa • UGIS show “pyloric dimple”.Congenital Gastric Outlet Obstruction • results from pyloric atresia and antral webs . uncommon. endoscopy • treatment is correction of dehydration and hypochloremic alkalosis. feeding difficulties and abdominal distention on 1st day of life • associated with polyhydramnios.

Peptic Ulcer in Children • Inflammation due to an imbalance between cytoprotective and cytotoxic factors in the stomach and duodenum. C-urea breath test and stool antigen test • Secondary: stress from sepsis. lesser curvature of the stomach • Primary: H. shock.pylori (serologic assay. drugs . gastritis and ulcerations • Endoscopy • Peptic ulcers: deep mucosal lesions that disrupts the muscularis mucosa of the gastric and duodenal wall.

dull or aching.) or Clarithromycin + Metronidazole + PPI • Antisecretory therapy: H2RAs. hematemesis or melena • Diagnosis: esophagogastroduodenoscopy • Management: H. cytoprotective agents . PPI.Peptic Ulcer: • Clinical manifestation: epigastric pain.) or Amoxicillin + Metronidazole (20mkd X 14days) + PPI (1mo. periumbilical. pylori gastritis: Amoxicillin (50mkd X 14days) + Clarithromycin (15mkd X 14days) + PPI (1mkd X 1 mo.

END OF 2ND SESSION .

atresia or stenosis • Extrinsic – compression of bowels by vessels.Intestinal Obstruction • Partial or complete. mucus production or tubular anatomy. frequent bilious vomiting with little or no distention. abdominal distention and obstipation • High: large volume. surgery . organs or cysts • Classic presentation: vomiting. obstipation • Low/distal: marked distention with vomiting (feculent). simple or strangulating (leads to bowel infarction and perforation). obstipation • Plain radiographs (upright and cross-table lateral views). intermittent pain. polyhydramnios • Intrinsic – inherent abnormalities of intestinal innervation. contrast studies (since colonic haustra are not fully developed) • Stabilize patient (fluid resuscitation).

malabsorption and protein-losing enteropathy .Malrotation • Inadequate mesenteric attachment of the intestines to the posterior abdominal wall. leaving the bowel vulnerable to volvulus or intestinal twisting (5th week to 12th week AOG) • Accompanied by congenital adhesions (Ladd bands) • 1st week of life: bilious emesis.

malposition of the Ligament of Treitz. corkscrew appearance of the small bowel and duodenal obstruction with “bird’s beak” appearance • Surgery . xray show gasless abdomen or duodenal obstruction with a double-bubble sign • UGIS – gold standard in evaluation. UTZ.Volvulus • Life-threatening complication of malrotation • Small bowel twists around the superior mesenteric artery • Contrast studies confirms diagnosis.

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Volvulus (“double bubble” sign) .

anemia . duct attenuates and separates from the intestine • Most common GI anomaly. painless rectal bleeding (lined by ectopic mucosa). lead point in intussusception. intraperitoneal bands • Outpouching of the ileum along the antimesenteric border 50- 75 cm from the ileocecal valve • Manifestations: 1st – 2nd yr of life. or the omphalomesenteric duct (provides nutrition until the placenta is established) or vitelline duct • 5th – 7th week. stool – brick or currant jelly colored.Meckel Diverticulum • Remnant of the embryonic yolk sac.

Meckel Diverticulum • Diagnosis: Meckel radionuclide scan (technetium-99m pertechnetate (plain xray and routine barium studies are of no value) • Diverticulitis • Surgical excision .

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leading to intestinal obstruction • Most common cause of lower intestinal obstruction in neonates. absence of ganglion cells in the submucosal and myenteric plexus (arrest of neuroblast migration from the proximal to the distal bowel) • Results to inadequate relaxation of the bowel wall and bowel wall hypertonicity.Congenital Aganglionic Megacolon (Hirschsprung Disease) • Developmental disorder (neurocristopathy) of the enteric nervous system. M>F .

abdominal tenderness. intestinal atresia • Older child: constipation. aureus. “ribbon-like” stools. sepsis and signs of bowel obstruction . difficile. S. consider “Currarino triad”: anorectal malformations. coliforms)diarrhea. bilious emesis or aspirates with feeding intolerance. failure to pass meconium. Differentials: meconium plug/ileus. sacral bone and presacral anomalies • Failure to pass stool dilatation of the proximal bowel distention  intraluminal pressure blood flow  deterioration of mucosal barrier  stasis and proliferation of bacteria (C. anaerobes.Congenital Aganglionic Megacolon (Hirschsprung Disease) • Neonatal period: distended abdomen.

Duhamel (create a neorectum). anorectal manometry (failure to relax of the internal anal sphincter). Swenson (excise aganglioninc segment and anastomose). stricture.Congenital Aganglionic Megacolon (Hirschsprung Disease) • Diagnosis: rectal suction biopsy (gold standard). Soave (endorectal pull-through (stripping the mucosa from the aganglionic rectum and bringing normally innervated colon through the muscular cuff) • Post-op problems: constipation. prolapse. fecal soiling . perianal abscess. recurrent enterocolitis. submucosa. unprepared contrast enema (barium) • Treatment of choice: laparoscopic single-stage endorectal pull-through procedure • Other operative interventions: 1. 2 cm above the dentate line. 3. > 1 month old. 2.

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adenovirus type C • Risk factors: GI infection (swelling of Peyer patches). M>F • Cause: idiopathic (90%). resp.pulls its mesentery • Most common cause of obstruction in 3mos – 6 yrs • Most common abdominal surgery in < 2yrs. intestinal polyp. lymphoid nodular hyperplasia (mucosal prolapse of the ileum into the colon). hemangioma.Intussusception • A portion of the alimentary tract is telescoped into an adjacent segment. neurofibroma. invanginates • Intussuscipiens: lower portion. intestinal duplication cyst. lymphoma. cystic fibrosis . ileocolic>cecocolic > ileoileal • Intussusceptum: upper portion of the bowel. lead points: Meckel diverticulum.

water soluble contrast media – “coiled-spring” sign • Treatment: radiologic hydrostatic reduction under fluoroscopic or ultrasonic guidance. weak and LETHARGIC • Triad: pain. bloody or currant-jelly stool • Diagnosis: UTZ . recurs. fatal if untreated . air. or resection with end-to-end anastomosis (ileoileal). hydrostatic (saline).Intussusception • Clinical manifestations: sudden onset of paroxysmal colicky pain. palpable sausage-shaped abdominal mass. straining efforts with legs and knees flexed and loud cries.

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Inflammatoy Bowel Disease
• Represent idiopathic chronic intestinal inflammation
• Onset: preadolescent/adolescent to young adulthood
• Genetic and Environmental influences
• Genes: NOD2 (1st IBD gene identified); IBD-5 risk
haplotype
• Pathogenesis: abnormality in intestinal mucosal
immunoregulation  abnormal rsponse to customary
enteric Ags or a normal response to a yet to-be identified
microbe  activation of mediators in inflammation 
tissue destruction and remodelling with fibrosis
• Crohn’s disease and Ulcerative colitis

Ulcerative Colitis
• Involves the colon (rectum and extends proximally)
• Ulcerative protitis and pancolitis
• Clinical manifestations: blood, mucus, pus in the stools;
diarrhea, tenesmus, urgency, crampy abdominal pain,
nocturnal BM
• Extraintestinal sumptom: pyodermal gangrenosum,
ankylosing spondylitis, Fe-deficiency anemia
• Fulminant colitis
• Differential diagnosis: dietary protein intolerance;
infectious colitis, H-S purpura
• Colon Ca - mucosal dysplasia

• Diagnosis: endoscopy and histologic findings
a. flexible sigmoidoscopy – can confirm the diagnosis
b. colonoscopy – extent of the disease; C/I: fulminant
colitis because of risk of toxic megacolon
c. barium enema – suggestive but not diagnostic
(“cut-off” demarcation”)
d. Fe-deficiency anemia, leukocytosis, hypoalbuminemia
e. biopsy – cryptitis, crypt abscesses, separation of crypts
by inflammatory cells, mucus depletion and branching
crypts
f. radiographs – loss of haustral markings in air-filled colon
(>6cm on diameter )

• Treatment: medical management – N/A; control
symptoms and reduce the risk
1. aminosalicylate – Sulfasalazine 50-75mkd (allergic rxn)
- Mesalamine 50mkg
- Balsalazide 110-175 mkd
2. probiotics – for maintenance of remission; prevents
pouchitis
3. prednisone – moderate to severe pancolitis; 1-2mkg; SE
4. Immunomodulators – Azathioprine 2-2.5mkg
- 6-mercatopurine 1-1.5mkg
5. Infliximab – Ab to tnf-α; induction and maintenance but SE

abdominal pain and low- grade fever • TPN vs.• Surgery – colectomy: intractable disease.colectomy with endorectal pull-through (J-pouch) . Enteral – no difference • Surveillance colonoscopy (8-10 yrs – colon Ca) .temporary ileostomy . complication of therapy. fulminant disease unresponsive to treatment .pouchitis – bloody diarrhea.

abdominal pain. penetrating . enterovesical. stomach. diarrhea.ileum and colon (ileocolitis) • 30% . hepatic abscess. growth failure. enterocolonic. duodenum) • 20% . vomiting.upper GI (esophagus.Crohn’s disease • Inflammatory process – eccentric and segmental with skip areas.colonic disease • Onset: teenage years • Clinical manifestations: inflammatory. “transmural” • 50% . stricturing. fistula formation (enteroenteric. easy fatigability. etc) . fever. malaise.

“cobblestone” appearance to the mucosal surface 2. radiologic – evidence of stricturing or penetrating disease 4.• Diagnosis: 1. loss of vascular patterns). friability. linear ulcers. endoscopy – inflammatory changes (eryhtema. low serum albumin. upper GI contrast study – choice for small bowel. fecal calprolectin or lactoferrin . nodularity and strictures 3. apthous ulcers. CBC.

Immunomodulators – azathioprine.tnf-α Ab (Infliximab – 0.• Treatment: medical management 1.6week infusions. Metronidazole – 10-20mkd – 1st line for perianal disease 3. 6-mercaptopurine if poor response to prednisone. Prednisone – especially for fistulas 4. Mesalamine 2.1. do PPD Adalimumab – subcutaneous • Enteral nutrition (elemental or polymeric diets) . not helpful acutely but has beneficial effect -methotrexate .

complications: bowel strictures.nutrition . endorectal pullthrough is discouraged because of recurrence • Prognosis: high morbidity.• Surgery: colectomy with conventional ileostomy (remove as limited a length as possible) is performed.Colonoscopy is done .surgery is unlikely to be curative (rate of reoperation is high and repeated surgeries lead to malabsorption due to short bowel syndrome_ . perianal disease. extraabdominal or retroperitoneal abscess .prevent osteopenia due to poor nutrition and use of corticosteroids . fistulas. low mortality .

End of 3rd Session .